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Background: Laryngocarcinoma (LC) is a common malignant tumor of the head and neck, accounting for 1% to 5% of human tumors. The primary objective of the present study was to evaluate the survival time of patients with LC at different sites. Methods: Information concerning patients with LC was extracted from the Surveillance, Epidemiology, and End Results (SEER) database between 1975 and 2016. Results: In total, 16 255 patients with LC were selected from the SEER database. Among all patients, 80.2% were male; males also predominated in each tumor site subgroup. Most of the patients were aged between 60 and 69 years, had white ethnicity, were single, and had American Joint Committee on Cancer (AJCC) stage I cancer with T1, N0, and M0. The present study investigated the role of interventions in all LCs at different AJCC stages. Across the whole population, regardless of the intervention used, survival increased in patients at any cancer site. Conclusions: The study found that male sex, age ≥80 years, black ethnicity, single status, T4, N4, M1, and AJCC stage IV were associated with higher mortality rates at all sites of LC. Aggressive interventions, especially surgery and radiotherapy, may improve survival in patients with LC at different sites and with different AJCC stages. [ABSTRACT FROM AUTHOR]

Objective To observe the clinical effect of Chinese medicine preparations at Shenque and Dazhui acupoints on relieving the symptoms of sleep disorders in patients with laryngocarcinoma. Methods A total of 50 hospitalized patients with laryngocarcinoma and sleep disorders were selected and randomly divided into treatment group (n=25) and control group(n=24, as one case lost to follow-up). In the treatment group, homemade herbal powders (the rhizome of Chinese goldthread and cinnamon) mixed with petroleum jelly and vinegar were applied to Dazhui and Shenque acupoints. In the control group, corn cobs and starch were used to make powder mixed with petroleum jelly and vinegar to make a placebo and then the same operation was performed to apply to the acupoints. The patient sleep quality was measured by using Pittsburgh Sleep Quality Index (PSQI) before treatment, after treatment and during follow-up. The Traditional Chinese Medicine (TCM) syndrome score of insomnia was compared between two groups, and the complication was recorded during treatment and follow-up. Results The total PSQI score decreased in both group after intervention and during follow-up, and the treatment group showed a significant reduction in total PSQI score compared with the control group (P＜0. 05). The TCM syndrome score decreased in both group after intervention, and TCM syndrome score in the treatment group was lower than that in the control group (P＜0. 05). One person in the treatment group experienced skin reaction. Conclusion Homemade Chinese medicine preparations applied externally to acupuncture points have relieved the symptoms of sleep disorders and improved the sleep quality of patients with laryngocarcinoma, which is worthy of promotion and application. (目的 观察中药制剂贴敷神阙和大椎改善喉癌患者睡眠障碍中的效果。方法 选取50例喉癌并发失眠的患者, 随机分入治疗组25例和对照组24例(脱落1例)。对照组给予常规护理并使用安慰剂贴敷神阙和大椎穴。治疗组则在常规护理的基础上采用黄连、肉桂中药粉剂掺入凡士林、陈醋赋形后贴敷于神阙、大椎穴。观察两组干预前后以及随访时匹兹堡睡眠量表(PSQI)得分, 比较两组干预前后失眠中医证候积分, 记录两组并发症发生情况。结果 干预后及随访时, 两组PSQI总分较干预前降低, 且治疗组PSQI总分均低于同期对照组, 差异有统计学意义(P＜0. 05)。干预后, 两组中医证候积分均降低, 且治疗组中医证候积分低于对照组, 差异有统计学意义(P＜0. 05)。对照组未发生不良反应事件, 治疗组仅出现1例皮肤发红症状。结论 自制黄连、肉桂中药制剂贴敷神阙、大椎穴可以有效改善喉癌患者失眠症状, 提高其睡眠质量, 值得临床推广运用。)

Introduction: Tumor exosome-derived miRNAs play important roles in the human laryngocarcinoma. However, it is still unknown if exosome miR-552 is involved in the laryngocarcinoma. The aim of the current study was to explore exosome miR-552's role in laryngocarcinoma and its underlying mechanisms. Methods: Hep-2 exosome was characterized by transmission electron microscopy and nanoparticle tracking technology. CCK-8 was used to determine cell viability, and a xenograft animal model was used to determine the tumorigenicity. qPCR and Western blotting were used to measure the changes in target biomarkers. Luciferase reporter assay was used to evaluate the interactions between miR-552 and PTEN. miRNA sequencing was used to check the changes in miRNA profiles. Results: miR-552 was upregulated in the laryngocarcinoma patients and was positively correlated to the cell proliferation and tumor growth. PTEN was identified as a direct target of miR-552. Hep-2 exosome is featured by high expression of miR-552 and treatment of Hep-2 exosome enhanced cell proliferation and tumorigenicity. The underlying mechanisms revealed that treatment of exosomes enhanced the malignant transformation of recipient cells in part by regulating epithelial-mesenchymal transition. Conclusion: Exosome miR-552 promotes laryngocarcinoma cells' malignant progression in part by the regulation of the PTEN/TOB1 axis. [ABSTRACT FROM AUTHOR]

Laryngocarcinoma is one of the most frequent malignancies occurring in the head and neck. The roles of spindle- and kinetochore-associated complex 1 (SKA1) in the malignant progression of several cancers have already been discussed. However, the precise significance and action's mechanism of SKA1 in laryngocarcinoma remain largely unknown. In this study, SKA1 was shown to be strongly expressed in laryngocarcinoma tissues and cells, and higher expression of SKA1 was associated with more severe tumor infiltration, larger tumor diameter, higher risk of lymphatic metastasis and later pathological stage. Additionally, loss-of-function assays in vitro suggested that SKA1 depletion caused a reduction in cell proliferation, migration, and colony formation as well as an increase in apoptosis. In animal experiments, tumors generated from AMC-HN-8 cells with SKA1 depletion exhibited declined tumor volume and weight. Similarly, the detection of Ki67 protein in xenograft tumor tissues reflected that knocking down SKA1 curbed tumor growth in vivo. Further exploration on downstream mechanism revealed that after treatment with Pifithrin-α, the suppression in proliferation level caused by SKA1 knockdown was reversed, while the increase of cell apoptosis was withdrawn; at the molecular level, Pifithrin-α treatment caused p-P53 and Bax diminished, while Bcl-2 ameliorated. In short, SKA1 promotes the development of laryngocarcinoma via activating the P53 signaling pathway. [ABSTRACT FROM AUTHOR]

Background and purpose: Laryngeal cancer is a refractory malignant tumor in otolaryngology. Radiotherapy and chemotherapy combined with surgery are often used, however, this treatment method has little improvement on the 5-year survival rate and mortality of patients, and is often accompanied by loss of laryngeal function and drug resistance. This study aimed to explore the effect of sonodynamic therapy (SDT) mediated by nanoacoustic sensitizer T-G-C particles on inhibiting human laryngeal cancer cells, and to provide a new non-invasive treatment for laryngeal cancer. Methods: Based on the synthesized T-G-C nanomaterials, the uptake of nanomaterials by Tu686 cells was evaluated under confocal laser scanning microscope, and the cell survival and apoptosis were evaluated by cell counting kit-8 (CCK-8) and Annexin Ⅴ- fluorescein isothiocyanate (FITC) reagent in the presence of ultrasound. BALB/c nude mouse xenograft model was established. The weight and tumor changes of mice were recorded during the treatment by injecting different types of drugs and ultrasonic irradiation in the tumor area, and the treatment effects were analyzed and compared. The apoptosis and necrosis of tumor cells and the production of reactive oxygen species (ROS) were compared by H-E, TUNEL, Ki-67 and DHE stainings. Results: Nanomaterials and cells incubated for 24 hours had no obvious toxicity, only led to the decline of cell survival rate under ultrasonic stimulation, and the cells showed mainly early apoptosis and late apoptosis. In the animal experiment, only after intratumoral injection of drugs and ultrasound treatment on the 1st, 3rd, 5th and 7th days, the tumor growth of mice in T-G-C+ultrasound group was significantly inhibited, and the tumor inhibition rate is 100%. After 16 d of treatment, obvious red fluorescence could be seen in the tumor area after ultrasound irradiation, which demonstrated that the core of tumor inhibition was the production of ROS. Conclusion: Biocompatible T-G-C nanoparticles stimulate the synergy of SDT and piezoelectric therapy when stimulated by ultrasound, and promote the early and late apoptosis of laryngeal cancer cells through ROS, which provides a combined treatment method for laryngeal cancer and promotes the application of multidisciplinary therapy in department of otolaryngology.

Laryngocarcinoma is a common malignancy in the upper respiratory tract. Enabled homolog (ENAH) is an actin-binding protein that is associated with the development of various cancers. However, its role and mechanism in laryngocarcinoma remain unknown. The ENAH level in laryngocarcinoma was examined in silico , in vitro and in vivo. The prognostic analysis of the ENAH level was assessed on laryngocarcinoma patients. Gain- and loss-of-function assays were conducted in AMC-HN-8 and TU686 cells. Sh-ENAH-containing AMC-HN-8 cells were implanted into naked mice. The role and mechanism of ENAH in laryngocarcinoma were investigated by CCK-8, transwell, immunofluorescence, dual luciferase, RT-qPCR, immunohistochemistry, and western blotting experiments. The ENAH level was upregulated in laryngocarcinoma, which predicted a poor prognosis in laryngocarcinoma patients. Gain- and loss-of-function results showed that ENAH promoted proliferation, invasion and EMT of laryngocarcinoma cells. Moreover, ENAH was transcriptionally activated by YY1, and YY1/ENAH axis enhanced these malignant progresses of laryngocarcinoma cells. Besides, ENAH activated the PI3K/AKT pathway, and 740Y-P abolished the accelerative role of ENAH in proliferation, invasion and EMT of laryngocarcinoma cells. Furthermore, knockdown of ENAH reduced tumor size and weight, and the expression level of vimentin and PI3K/AKT pathway in tumor-bearing mice. ENAH transcriptionally activated by YY1 promotes cell growth, invasion and EMT of laryngocarcinoma through the activation of PI3K/AKT signaling. [Display omitted] • High expression of ENAH in laryngocarcinoma predicted a poor prognosis. • ENAH promoted growth, invasion and EMT of laryngocarcinoma cells. • ENAH was transcriptionally regulated by YY1. • YY1/ENAH axis regulated the growth, invasion and EMT of laryngocarcinoma cells. • ENAH promoted the malignant progression of laryngocarcinoma via PI3K/AKT pathway. [ABSTRACT FROM AUTHOR]

Background and purpose: Laryngeal cancer is a refractory malignant tumor in otolaryngology. Radiotherapy and chemotherapy combined with surgery are often used, however, this treatment method has little improvement on the 5-year survival rate and mortality of patients, and is often accompanied by loss of laryngeal function and drug resistance. This study aimed to explore the effect of sonodynamic therapy (SDT) mediated by nanoacoustic sensitizer T-G-C particles on inhibiting human laryngeal cancer cells, and to provide a new non-invasive treatment for laryngeal cancer. Methods: Based on the synthesized T-G-C nanomaterials, the uptake of nanomaterials by Tu686 cells was evaluated under confocal laser scanning microscope, and the cell survival and apoptosis were evaluated by cell counting kit-8 (CCK-8) and Annexin Ⅴ-fluorescein isothiocyanate (FITC) reagent in the presence of ultrasound. BALB/c nude mouse xenograft model was established. The weight and tumor changes of mice were recorded during the treatment by injecting different types of drugs and ultrasonic irradiation in the tumor area, and the treatment effects were analyzed and compared. The apoptosis and necrosis of tumor cells and the production of reactive oxygen species (ROS) were compared by H-E, TUNEL, Ki-67 and DHE stainings. Results: Nanomaterials and cells incubated for 24 hours had no obvious toxicity, only led to the decline of cell survival rate under ultrasonic stimulation, and the cells showed mainly early apoptosis and late apoptosis. In the animal experiment, only after intratumoral injection of drugs and ultrasound treatment on the 1st, 3rd, 5th and 7th days, the tumor growth of mice in T-G-C+ultrasound group was significantly inhibited, and the tumor inhibition rate is 100%. After 16 d of treatment, obvious red fluorescence could be seen in the tumor area after ultrasound irradiation, which demonstrated that the core of tumor inhibition was the production of ROS. Conclusion: Biocompatible T-G-C nanoparticles stimulate the synergy of SDT and piezoelectric therapy when stimulated by ultrasound, and promote the early and late apoptosis of laryngeal cancer cells through ROS, which provides a combined treatment method for laryngeal cancer and promotes the application of multidisciplinary therapy in department of otolaryngology. [ABSTRACT FROM AUTHOR]

Abstract Background LOXL1-AS1 is a long non-coding RNA (lncRNA) that plays crucial roles in various cancers. However, the functional role of LOXL1-AS1 in laryngocarcinoma remains unclear. Thus we planned to probe into the function and underlying mechanism of LOXL1-AS1 in laryngocarcinoma. Methods Gene expression was evaluated in laryngocarcinoma cells using RT-qPCR. The ability of cell proliferation and migration was assessed by CCK8, colony formation, wound healing and transwell assays. The interaction among LOXL1-AS1, miR-589-5p and TRAF6 was detected by Ago2-RIP, RNA pull down and luciferase reporter assays. Results LOXL1-AS1 was overexpressed in laryngocarcinoma cells. Silencing of LOXL1-AS1 suppressed cell proliferation, migration and EMT in laryngocarcinoma. Moreover, miR-589-5p, the downstream of LOXL1-AS1, directly targeted TRAF6 in laryngocarcinoma. Importantly, LOXL1-AS1 augmented TRAF6 expression in laryngocarcinoma cells by sequestering miR-589-5p. Besides, miR-589-5p worked as a tumor-inhibitor while TRAF6 functioned as a tumor-facilitator in laryngocarcinoma. Of note, rescue experiments both in vitro and in vivo validated that LOXL1-AS1 aggravated the malignancy in laryngocarcinoma by targeting miR-589-5p/TRAF6 pathway. Conclusions LOXL1-AS1 promotes the proliferation and migration of laryngocarcinoma cells through absorbing miR-589-5p to upregulate TRAF6 expression.

Xiaoting Zhao,1,2 Mei Jiang,1,2 Ziyu Wang,2 Xiaohong Chen,3 Hongzhen Wang,4 Wentao Yue,1 Chao Cai5,6 1Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Cellular and Molecular Biology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Tongzhou, Beijing, People’s Republic of China; 3Department of Otolaryngology, Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, People’s Republic of China; 4Department of Oncology, Rizhao City Hospital of Traditional Chinese Medicine, Rizhao, Shandong, People’s Republic of China; 5Beijing YouAn Hospital, Capital Medical University, Beijing, People’s Republic of China; 6Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Tongzhou, Beijing, People’s Republic of ChinaCorrespondence: Chao Cai; Wentao Yue Email fangzecai@126.com; yuewt@ccmu.edu.cnBackground: Laryngeal carcinoma is a common cancer among head and neck tumors, accounting for 0.5– 1% new cancer cases or deaths of all tumors throughout the body. Despite improvements in diagnostic and therapy, the prognosis of laryngeal carcinoma patients still remains poor. Thus, it is very important to identify the biomarkers involved in the molecular pathogenesis of laryngeal carcinoma. Cyclin Y (CCNY) is a conserved cell cycle regulator that acts as a growth factor in many cancers. The clinical significance of CCNY in laryngeal carcinoma remains unknown. The function of CCNY in laryngocarcinoma was studied in this paper.Materials and Methods: CCNY knock-out cells were constructed by CRISPR/CAS9 technique. CCNY overexpression cells were also constructed based on CCNY knock-out cells. Cell growth ability was detected by MTS assay, high-content cell analysis, colony formation assays, and anchorage-independent growth assays. The protein levels in laryngocarcinoma cells were determined by Western blot. The role of CCNY in cell cycle progression was evaluated by flow cytometry.Results: CCNY knock-out cells and CCNY up-regulation cell models were obtained successfully. Suppression of CCNY expression inhibited Hep2 cell growth. Cell growth was enhanced by the up-regulation of CCNY. The percentage of cells in G1 phase was altered when CCNY expression was down-regulated or up-regulated. The phosphorylation level of MEK and ERK as well as cyclin E protein level was also regulated by the expression level of CCNY.Conclusion: In laryngocarcinoma cell line Hep2 cells, cell proliferation was controlled by CCNY. The expression of CCNY was involved in the cell cycle progress of Hep2 cells. It indicated that CCNY could promote cell growth by activating MEK/ERK/cyclin E signaling pathway.Keywords: laryngocarcinoma, CCNY, cell cycle, ERK, cyclin E

Yigang Wang,1 Binrong Wang,1 Junnan Liang,2 Caixia Cui,3 Chang Ying,1 Fang Huang,4 Buyun Ma,1 Xiumei Zhou,1 Liang Chu21College of Life Sciences, Zhejiang Sci-Tech University, Hangzhou 310018, People’s Republic of China; 2Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People’s Republic of China; 3Department of Otorhinolaryngology, Affiliated Hospital of Hangzhou Normal University, Hangzhou 310015, People’s Republic of China; 4Department of Pathology, Zhejiang Provincal People’s Hospital, Hangzhou 310014, People’s Republic of ChinaBackground: Oncolytic virus can specifically replicate in and then lyse tumor cells, but seldom in normal cells. Further studies have shown the significant therapeutic effect of oncolytic virotherapy combining with other strategies, such as chemo-, radio-, and immunotherapy et al. In this study, we investigated the combinational effect of oncolytic virus ZD55-TRAIL and chemotherapy drug doxorubicin (DOX) on human laryngeal squamous cell carcinoma (LSCC).Methods: The effect of ZD55-TRAIL combined with DOX on cell growth was assessed in LSCC Hep2 cells and normal cells by MTT assay. Hochest 33342 staining was performed to observe cell morphological changes. Western blot was used to detect the expression of apoptotic activation proteins. The in vivo antitumor efficacy of combination treatment was estimated in laryngeal cancer xenograft models.Results: The combination of ZD55-TRAIL and DOX exhibited enhanced inhibitory effects on laryngocarcinoma cell growth, and had few side effects to normal cells in vitro. Chemotherapy drug increased the inducement of tumor cell apoptosis mediated by oncolytic virus. In vivo experiment confirmed that the combination treatment significantly inhibited Hep2 laryngocarcinoma xenografts growth in mice.Conclusion: The oncolytic viro-chemotherapy is a potent therapeutic approach for in vitro cytotoxicity evaluation of Hep2 cells and xenograft growth in vivo.Keywords: laryngocarcinoma, oncolytic virus, ZD55-TRAIL, doxorubicin

Background: Laryngocarcinoma is the most frequent head and neck malignant tumor. MALAT1 have a role in promoting cell proliferation and metastasis in several tumors. This research aimed to investigate the great roles of MALAT1in laryngocarcinoma. Methods: Overall, 54 cases of laryngocarcinoma tissues pathological specimens and paracancerous tissues were collected by surgical resection from the Department of Otolaryngology-Head and Neck Surgery at the Shandong Provincial Hospital affiliated to Shandong University, China from Jan 2012 to Oct 2015. The microRNA and protein levels of genes were evaluated by RT-qPCR and western blot. The proliferative and invasive ability were calculated usingCCK8 and transwell assays. Kaplan-Meier method was used to assess the survival of laryngocarcinoma patients. Results: In laryngocarcinoma tissues and cells, lncRNA MALAT1 expression was significantly increased compared to normal tissues and cells. LncRNA MALAT1 promotes proliferation and migration of laryngocarcinoma cells. LncRNA MALAT1 upregulates HMGA1 expression by acting as a competitive endogenous RNA (ceRNA) for miR-125b. Rescue experiments showed that microRNA-125b inhibitor reversed the change in cell viability and invasion induced by sh-MALAT1. Down regulation of lncRNA MALAT1 inhibits laryngocarcinoma proliferation and invasion by modulating miR-125b /HMGA1. Conclusion: LncRNA MALAT1 promotes the development of laryngocarcinoma by regulating the expression level of HMGA1 by acting as a miR-125b ceRNA and may be considered as a new strategy for the development of laryngocarcinoma.

circRNAs have been shown to be involved in cancer progression. It is unclear whether circPGAM1 exerts its effect on laryngocarcinoma drug resistance. In this study, we employed colony formation and MTT assay to determine colony number and cell viability under cisplatin treatment. TUNEL experiment was used to evaluate apoptosis of laryngocarcinoma cells in the presence of cisplatin. Xenograft tumor experiment was performed to assess in vivo tumor growth of SNU46 cells. We found that circPGAM1 enhanced colony formation and viability of SNU46 and M4E cells. In contrast, circPGAM1 caused attenuated cell apoptosis. Furthermore, we also confirmed that circPGAM1 played a key role in tumor growth in animal model and clinical patients. miR-376a was identified and proved to act as key effector for circPGAM1-mediated drug resistance. Finally, autophagy-related gene ATG2A was shown to rescue miR-376a-modulated drug resistance of laryngocarcinoma cells. Herein, we illuminate the role of circPGAM1 in laryngocarcinoma drug resistance, thereby facilitating development of targeted therapy for treating laryngocarcinoma. • circPGAM1 promoted drug resistance of laryngocarcinoma. • circPGAM1 contributed to laryngocarcinoma progression in animal model and clinical setting. • miR-376a rescued circPGAM1-mediated drug resistance of laryngocarcinoma. • Autophagy served as downstream effector for miR-376a-suppressed drug resistance of laryngocarcinoma. [ABSTRACT FROM AUTHOR]

Background: LOXL1-AS1 is a long non-coding RNA (lncRNA) that plays crucial roles in various cancers. However, the functional role of LOXL1-AS1 in laryngocarcinoma remains unclear. Thus we planned to probe into the function and underlying mechanism of LOXL1-AS1 in laryngocarcinoma. Methods: Gene expression was evaluated in laryngocarcinoma cells using RT-qPCR. The ability of cell proliferation and migration was assessed by CCK8, colony formation, wound healing and transwell assays. The interaction among LOXL1-AS1, miR-589-5p and TRAF6 was detected by Ago2-RIP, RNA pull down and luciferase reporter assays. Results: LOXL1-AS1 was overexpressed in laryngocarcinoma cells. Silencing of LOXL1-AS1 suppressed cell proliferation, migration and EMT in laryngocarcinoma. Moreover, miR-589-5p, the downstream of LOXL1-AS1, directly targeted TRAF6 in laryngocarcinoma. Importantly, LOXL1-AS1 augmented TRAF6 expression in laryngocarcinoma cells by sequestering miR-589-5p. Besides, miR-589-5p worked as a tumor-inhibitor while TRAF6 functioned as a tumor-facilitator in laryngocarcinoma. Of note, rescue experiments both in vitro and in vivo validated that LOXL1-AS1 aggravated the malignancy in laryngocarcinoma by targeting miR-589-5p/TRAF6 pathway. Conclusions: LOXL1-AS1 promotes the proliferation and migration of laryngocarcinoma cells through absorbing miR-589-5p to upregulate TRAF6 expression. [ABSTRACT FROM AUTHOR]

Recently, abundant evidence has clarified that long noncoding RNAs (lncRNAs) play an oncogenic or anticancer role in the tumorigenesis and development of diverse human cancers. Described as a crucial regulator in some cancers, MIR22HG has not yet been studied in laryngocarcinoma and therefore the underlying regulatory role of MIR22HG in laryngocarcinoma is worth detecting. In this study, MIR22HG expression in laryngocarcinoma cells was confirmed to be downregulated, and upregulated MIR22HG expression led to suppressive effects on laryngocarcinoma cell proliferation and migration. Molecular mechanism assays revealed that MIR22HG sponges miR-5000-3p in laryngocarcinoma cells. Besides, decreased expression of miR-5000-3p suppressed laryngocarcinoma cell proliferation and migration. Moreover, the FBXW7 gene was reported to be a downstream target gene of miR- 5000-3p in laryngocarcinoma cells. More importantly, rescue assays verified that FBXW7 depletion or miR-5000-3p upregulation countervailed the repressive effects of MIR22HG overexpression on laryngocarcinoma progression. In addition, E2F6 was proved to be capable of inhibiting MIR22HG transcription in laryngocarcinoma cells. To sum up, E2F6-induced downregulation of MIR22HG promotes laryngocarcinoma progression through the miR-5000-3p/FBXW7 axis. [ABSTRACT FROM AUTHOR]

For the exploration of circular RNA light chain kinase (circRNA-MYLK), siRNA#1 and siRNA#2 targeting circRNA-MYLK as well as microRNA(miR)-145-5p inhibitor were transfected. Viability was valued with the CCK-8. The protein expression was examined relying on Western blot. The expression of circRNA-MYLK or miR-145-5p was tested depending on qRT-PCR. The apoptotic/migration/invasion rate was separately measured by the Annexin v-FITC/PI with flow cytometer or chambers assays. CircRNA-MYLK was overexpressed in tumor tissue. Silencing circRNA-MYLK induced the inhibitions of viability, invasion and migration, as well as the blocks of MEK/ERK and NF-κB cascades, however, silencing circRNA-MYLK led to provoking of apoptosis. Besides, circRNA- MYLK silencing stimulated the over-production of miR-145-5p, whose silencing abolished the effects of siRNA#1 and siRNA#2 of circRNA-MYLK on those factors above. The circRNA-MYLK had oncogenic roles via targeting miR-145-5p in the Hep-2 cell line via stimulating MEK/ERK and NF-κB cascades. [ABSTRACT FROM AUTHOR]

Numerous researches show that MicroRNAs (miRNAs) participate in tumorigenesis, progression, recurrence and drug resistance of malignant tumors, including laryngocarcinoma. miR-552 works as an oncogene in both colorectal cancer and liver cancer. However, the potential role of miR-552 in laryngocarcinoma is unknown. Herein, we for first found that miR-552 expression was upregulated in laryngocarcinoma tissues compared with their normal controls. Moreover, miR-552 expression was also increasing in the laryngocarcinoma cells. miR-552 interference inhibited the proliferation and metastasis of laryngocarcinoma cells in vitro and in vivo. Mechanically, bioinformatics and luciferase reporter analysis identified p53 as a direct target of miR-552. miR-552 knockdown upregulated the p53 mRNA and protein expression in laryngocarcinoma cells. miR-552 expression was negatively associated with p53 expression in laryngocarcinoma tissues. More importantly, the p53 siRNA or p53 overexpression virus abrogated the discrepancy of growth and metastasis capacity between miR-552 interference laryngocarcinoma cells and control cells. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study aims to investigate whether inflammatory response or oxidative stress could induce upregulation of PTPN2, thus promoting the progression of laryngocarcinoma. PATIENTS AND METHODS: PTPN2 levels in laryngocarcinoma tissues and normal tissues were detected. In addition, PTPN2 levels in laryngocarcinoma tissues with stage 1/2 or stage 3/4 were determined as well. In vitro abundance of PTPN2 was measured in laryngocarcinoma cells and immortalized human nasopharyngeal epithelial cells. Survival analysis was conducted in laryngocarcinoma patients with high or low expression level of PTPN2. Subsequently, M4E cells were stimulated with inflammation (IFN-γ or TNF-a treatment) or oxidative stress (H2O2 stimulation), followed by determination of the protein level of PTPN2. In M4E cells stimulated with different concentrations of H2O2, the clonality and Ki-67 positive cell ratio were detected. Finally, clonality and Ki-67 positive cell ratio in M4E cells transfected with negative control or sh-PTPN2, regardless of H2O2 stimulation, were assessed. RESULTS: PTPN2 was upregulated in laryngocarcinoma tissues, especially those in stage 3/4. Similarly, in vitro abundance of PTPN2 was higher in laryngocarcinoma cell lines. The high level of PTPN2 predicted poor prognosis in laryngocarcinoma patients. IFN-γ or TNF-α treatment upregulated the protein level of PTPN2. Meanwhile, H2O2 stimulation upregulated the protein level of PTPN2, dose-dependently increased clonality, and Ki-67 positive cell ratio in M4E cells. The knockdown of PTPN2 suppressed clonality and Ki-67 positive cell ratio in M4E cells stimulated by H2O2 or not. CONCLUSIONS: Inflammatory response or oxidative stress could induce upregulation of PTPN2, thus promoting the proliferative ability of laryngocarcinoma. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Laryngocarcinoma is one of the most ordinary head and neck cancers worldwide. Recent studies have revealed that circular RNAs (circRNAs) act as an important role in malignant tumors and participate in tumorigenesis. The purpose of our work is to uncover how hsa_circ_0000285 functions in laryngocarcinoma. PATIENTS AND METHODS: In this research, the Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to monitor hsa_circ_0000285 expression in laryngocarcinoma samples. Besides, function assays were performed in laryngocarcinoma cells transfected with hsa_circ_0000285 shRNA or lentivirus. Furthermore, the RT-qPCR and Western blot assay were conducted to explore the target-signaling pathway of hsa_circ_0000285. RESULTS: Hsa_circ_0000285 expression was found to be upregulated in laryngocarcinoma samples compared with adjacent tissues. The function assays showed that the inhibition of the cell proliferation was induced via knockdown of hsa_circ_0000285 in laryngocarcinoma in vitro, while the promotion of cell apoptosis was induced via the knockdown of hsa_ circ_0000285 in laryngocarcinoma in vitro. On the other hand, the overexpression of hsa_ circ_0000285 had the opposite function. In addition, the Wnt/β-catenin signaling pathway was repressed via knockdown of hsa_circ_0000285 in laryngocarcinoma, while the Wnt/β-catenin signaling pathway was promoted via overexpression of hsa_circ_0000285 in laryngocarcinoma. CONCLUSIONS: In our study, hsa_circ_0000285 was first identified as a novel oncogene and could induce the Wnt/β-catenin signaling pathway in laryngocarcinoma. [ABSTRACT FROM AUTHOR]

Glucose Transporter-1 (GLUT-1) is considered to be a possible intrinsic marker of hypoxia in malignant tumors, which is an important factor in radioresistance of laryngocarcinoma. We speculated that the inhibition of GLUT-1 expression might improve the radiosensitivity of laryngocarcinoma. GLUT-1 siRNA was designed to inhibit the GLUT-1 expression, but the high molecular weight and difficult drug delivery limited the application. Herein, we constructed a glycolipid polymer chitosan oligosaccharide grafted stearic acid (CSSA) to conjugate siRNA via electrostatic interaction. The characteristics of CSSA and CSSA/siRNA were studied, as well as the radiosensitization effect of siRNA on human laryngocarcinoma epithelial (Hep-2) cells. Compared with the traditional commercial vector LipofectamineTM2000 (Lipo), CSSA exhibited lower cytotoxicity, more efficiently cellular uptake. Incubating with CSSA/siRNA, the survival rates of Hep-2 cells were significantly decreased comparing with either the group before transfection or Lipo/siRNA. CSSA is a promising carrier for efficient siRNA delivery and radiosensitization of laryngocarcinoma.

OBJECTIVE: The poor prognosis of advanced laryngocarcinoma was associated with the epithelial-mesenchymal transformation (EMT), which was related to the dysregulated expression of free fatty acids receptor 4 (FFAR4). By detecting the expression of FFAR4 in laryngocarcinoma and its relation with the clinicopathological characteristics and prognosis of laryngocarcinoma, as well as conducting in vitro experiments, our aim is to explore the role of FFAR4 in laryngocarcinoma biological and clinical process. PATIENTS AND METHODS: The protein expression level of FFAR4 in 54 cases of laryngocarcinoma and 30 cases of laryngocarcinoma adjacent tissues was detected by immunohistochemistry. Combined with clinical follow-up data, the Kaplan-Meier survival curve and log-rank test were conducted to compare the relation between the expression of FFAR4, the clinicopathological characteristics, and the 5-year survival rate in laryngocarcinoma. Multivariable Cox regression analysis revealed the independent predictors for the prognosis of laryngocarcinoma. CCK-8 and migration assay were used to test cell proliferation and migration abilities. RESULTS: FFAR4 was upregulated in laryngocarcinoma tissues and influenced cell proliferation and migration abilities. The FFAR4 expression was related to the age and lymph node metastasis in laryngocarcinoma patients and indicated a reduced 5-year survival rate and increased lymph node metastasis. CONCLUSIONS: The upregulation FFAR4 expression was associated with the lymph node metastasis and the prognosis. FFAR4 can significantly promote laryngocarcinoma cell proliferation and migration in vitro. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Long noncoding RNAs (lncRNAs) have been reported to participate in the progression and development of many human diseases. In this study, we are committed to uncover the potential function of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in the development of laryngocarcinoma. PATIENTS AND METHODS: LncRNA NEAT1 expression in laryngocarcinoma cells and 54 paired laryngocarcinoma samples was detected by Real-time quantitative polymerase chain reaction (RT-qPCR). Furthermore, the regulatory effects of NEAT1 on the proliferation and metastasis of laryngocarcinoma cells were evaluated. Biological role of NEAT1/miR-29a-3p axis was finally explored in regulating the progression of laryngocarcinoma. RESULTS: NEAT1 was upregulated in laryngocarcinoma tissues and cell lines. NEAT1 knockdown suppressed growth and invasive abilities in laryngocarcinoma cells, while overexpression of NEAT1 enhanced such abilities. Further experiments showed that miR-29a-3p was directly targeted by NEAT1, and participated in NEAT-mediated progression of laryngocarcinoma. CONCLUSIONS: NEAT1 is a novel oncogene in laryngocarcinoma and could enhance growth and invasion of laryngocarcinoma cells by targeting miR-29a-3p. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Many studies have recently suggested that dendritic cell (DC) vaccine contributes to the immunotherapy of various types of human tumors. It has been proved that the tumor antigen sensitizing and the gene silencing are effective methods for the preparation of the DC vaccines. The aim of this study is to investigate the specific anti-laryngocarcinoma immune response for the suppression of cytokine signaling1 (SOCS1) silencing and Hep- 2 sensitizing DC. MATERIALS AND METHODS: The dendritic cells derived from peripheral blood mononuclear cells were induced by cytokines GM-CSF, IL-4, and TNF-α in vitro, and the morphological characteristics of dendritic cells were observed under a microscope, indicating that they successfully differentiated into dendritic cells. The RNA interference vector was used to transfect dendritic cells. The expression of SOCS1 was detected by Western blot and the effective target sequence for inhibiting the expression of SOCS1 was screened. The expressions of CD83, CD86, and HLA-DR on dendritic cells were detected by flow cytometry. The content of IFN-γ in the supernatant was analyzed by enzyme-linked immunosorbent assay (ELISA). Methyl thiazolyl tetrazolium (MTT) was used to evaluate the ability of dendritic cells to stimulate T cell proliferation and induce the killing activity of cytotoxic T cells. RESULTS: The result of PCR and Western blot analysis shows that the expression of SOCS1 significantly decreased under the influence of the 5th interference sequence. The flow cytometric analysis results show that SOCS1 silencing and Hep-2 sensitizing dendritic cells had high expressions of CD83 (85.61±0.96)%, CD86 (96.86±1.20)%, and HLA-DR (98.02±0.94)%. The DC vaccine could increase the production of IFN-γ according to the ELISA assay results. The MTT assay results show that the DC vaccine could also stimulate the proliferation of the T cells and effectively and eventually enhance the specific killing effect of CTL. CONCLUSIONS: SOCS1 silencing and Hep-2 sensitizing DC vaccine could induce an effective and specific anti-laryngocarcinoma immune response. [ABSTRACT FROM AUTHOR]

Abstract Aberrant expression of RBM6 has been implicated in the development of human malignancies. However, the bio-function of RBM6 in laryngocarcinoma is still almost blank. Here we identified that RBM6 was downregulated in laryngocarcinoma tissues, as well as laryngocarcinoma cell lines. Notably, the expression level of RBM6 was lower in laryngocarcinoma patients at stage3/4 than that in laryngocarcinoma patients at stage1/2. Upregulation of RBM6 suppressed the proliferation of TU212 and Hep-2 cells, as shown by decreased cell viability and Ki67 level. In parallel, overexpression of RBM6 inhibited invasion and promoted apoptosis of TU212 and Hep-2 cells, as evidenced by downregulation of MMP-2 and MMP-9 protein expression and upregulation of cleaved caspase-3 protein expression. In vivo , RBM6 overexpression repressed the laryngocarcinoma tumor growth. EGFR mRNA level was higher in the laryngocarcinoma tissues than that in the adjacent normal tissues. Moreover, upregulation of RBM6 reduced the expression of EGFR, ERK and p-ERK in vitro and in vivo. Our data suggest that RBM6 as a tumor suppressor represses the growth and progression in laryngocarcinoma. Highlights • RBM6 is downregulated in laryngocarcinoma cells and tissues. • Upregulation of RBM6 suppresses proliferation in TU212 and Hep-2 cells. • Upregulation of RBM6 inhibits invasion and promotes apoptosis in TU212 and Hep-2 cells. • Upregulation of RBM6 inhibits laryngocarcinoma tumor growth. • Upregulation of RBM6 suppresses the EGFR-associated signaling pathway. [ABSTRACT FROM AUTHOR]

The pharmacological actions of Ophiopogonin D include resistance to cardiovascular and cerebrovascular diseases, anti-aging effects, improvement in learning deficit and dysmnesia, anti-tumor, anti-radiation and anti-inflammatory effects, immunoregulation, and the relief of cough and hepatopulmonary pathological lesions. However, the efficacy of Ophiopogonin D on human laryngocarcinoma remains to be elucidated. The present study therefore investigated whether the anti-cancer effect of Ophiopogonin D inhibits cell proliferation and induces apoptosis of human laryngocarcinoma. In the present study, it was found that Ophiopogonin D inhibited cell proliferation, promoted cytotoxicity, induced apoptosis and increased caspase-3/9 activity in human laryngocarcinoma cells. Ophiopogonin D significantly suppressed cyclin B1 and matrix metalloproteinase-9 (MMP-9) protein expression, and upregulated p-p38 MAPK protein expression in human laryngocarcinoma cells. Together, these results suggest Ophiopogonin D inhibits cell proliferation and induced apoptosis in human laryngocarcinoma cells through downregulation of cyclin B1 and MMP-9 and upregulation of the p38 MAPK signaling pathway. Therefore, Ophiopogonin D may be a potential therapy for the treatment of human laryngocarcinoma. [ABSTRACT FROM AUTHOR]

Epidermal growth factor receptor (EGFR), cyclin D1 and KRAS proto-oncogene, GTPase (KRAS) genes serve roles in the occurrence and development of tumors. The aim of the current study was to investigate the expression levels of EGFR, cyclin D1 and KRAS in laryngocarcinoma tissues and their association with clinical features. In addition, correlation between the expression levels of EGFR, cyclin D1 and KRAS was analyzed in laryngocarcinoma tissues. The expression levels of EGFR, cyclin D1 and KRAS in 46 patients with laryngocarcinoma and 20 patients with vocal cord polyps as the control group were determined using Super Vision immunohistochemical staining assay kits. The differences in clinical and pathological parameters between groups were statistically analyzed using SPSS software version 16.0. The expression rates of EGFR, cyclin D1 and KRAS were 71.7, 52.2 and 39.1%, respectively in laryngocarcinoma tissues, and 10.0, 5.0 and 10.0%, respectively in vocal cord polyps. There was a positive correlation between the expression levels of EGFR, cyclin D1 and KRAS. The expression of these genes was also closely associated with the clinical stage, treatment response and prognosis of patients with laryngocarcinoma. Multivariate analysis of prognosis using the Cox regression model indicated that EGFR expression in laryngocarcinoma tissues and the clinical stage of patients with laryngocarcinoma were closely associated with patient prognosis. The results of the current study indicated that EGFR, cyclin D1 and KRAS were synergistically involved in the occurrence and development of laryngocarcinoma, directly affecting the prognosis of patients. Additionally, high expression of EGFR, cyclin D1 and KRAS facilitated the invasion and metastasis of laryngocarcinoma cells. The expression of EGFR in laryngocarcinoma tissues and clinical stage were two independent risk factors affecting the prognosis of patients. [ABSTRACT FROM AUTHOR]

Head and Neck Cancer (HNC), including tumors in oral cavity, pharyngeal, nasal cavity and laryngeals, which has a high prevalence and complex pathogenesis. Whereas, laryngocarcinoma is the world's sixth common form of malignant tumors and accounts for over 3% of malignant HNCs. Therefore, laryngocarcinoma should be given particular attention in HNCs. Human papillomavirus (HPV) belongs to small double strands DNA virus. Previous studies have reported that HPV infection is associated with the occurrence and the prognosis of different tumors. Recently, the role of HPV infection to the carcinogenesis and clinical significance of HNC, especially to tumors in pharynx oralix has attracted a variety of scholars' concern. However, the role of HPV infection to laryngocarcinoma has not been defined. We reviewed the correlation of HPV infection and laryngocarcinoma, and the potential carcinogen effects of HPV infection. Although there were differences in the relevance ratio of HPV infection in laryngocarcinoma in different research teams, preliminary studies have indicated that the infection of high risk HPV subtypes, such HPV 16 and HPV 18, exist a certin correlation of the occurrence rate of laryngocarcinoma. DNA of HPV virus integrates with the tumor cells, and the expression of p16 was higher in laryngocarcinoma cells. But the prevention and accurate treatment of diseases caused by HPV infection remains unclear, further research is required to clarify the mechanism underlying HPV infection involvement in HNC. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) are known to play a regulatory role in various cancers including laryngocarcinoma. MiR-29a-3p is a potential tumor-suppressive miRNA, but its function in laryngocarcinoma is unknown. The purpose of this study was to investigate the roles of miR-29a-3p in laryngocarcinoma. Prominin1 (PROM1) was predicted as a target gene of miR- 29a-3p and this was verified using a luciferase reporter assay. Transfection of miR-29a-3p into two laryngocarcinoma cell lines indicated that miR- 29a-3p could decrease cell proliferation and enhance the chemotherapy response by targeting PROM1. PROM1 expression was up-regulated in the laryngocarcinoma cells when miR-29a-3p was down-regulated. We found miR-29a-3p expression levels were lower in laryngocarcinoma tissues than in control tissues. We also found that miR-29a-3p expression was negatively correlated with PROM1 expression in laryngocarcinoma tissues. The study demonstrates that miR-29a-3p suppresses cell proliferation in laryngocarcinoma by targeting PROM1. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) play important roles in gene regulation during laryngocarcinoma. MiR-9 is a potential oncomiR, but its function in laryngocarcinoma is not known. The aim of this study is to investigate the roles of miR-9 in laryngocarcinoma. We found miR-9 expression was higher in laryngocarcinoma tissues compared with their normal controls, so did the laryngocarcinoma cells. Cellular function of miR-9 indicated that miR-9 restoration in laryngocarcinoma cells could promote cell proliferation and metastasis. Phosphatase and tensin homolog (PTEN) was predicted as a target gene of miR-9 and verified using luciferase reporter assay. PTEN expression was down-regulated in the laryngocarcinoma cells with miR-9 overexpression. We also found that miR-9 expression was negatively associated with PTEN expression in laryngocarcinoma tissues. [ABSTRACT FROM AUTHOR]

Myoepithelial carcinoma of the head and neck is a rare malignant tumor that usually arises from the salivary glands but rarely from the larynx. Here, we describe 11 cases (one treated by us and 10 previously published) of laryngeal myoepithelial carcinoma. Our patient was a 60-year-old male who initially presented with hoarseness and throat pain. The patient had suffered from continuing hoarseness and throat pain for one month before he consulted an otorhinolaryngologist. Computed tomography (CT) scan showed a polypoid tumor involving the right vocal cords. Biopsy was performed, and the disease was pathologically diagnosed as myoepithelial carcinoma of the larynx by hematoxylin-eosin and immunohistochemical staining. The total follow-up period was 15 months. Repeated laryngoscopies or CT scans revealed no recurrence or residual lesion during the post-surgical course., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Initiation of apoptosis is an important event for chemoprevention and chemotherapy of cancer. Naturally derived products had drawn growing attention as lead compounds for anticancer drug discovery. ABL-L, a semisynthetic analogue of natural sesquiterpenoid 1- O -acetylbritannilactone (ABL) isolated from Inula britannica , showed stronger suppression against three solid tumor cell lines with 4–10 fold improvement than ABL. However, its molecular mechanism of cell death induction has still not been determined. The present study evaluated the anticancer efficacy of ABL-L and its biological activities mechanism on human laryngocarcinoma cells HEp-2 in vitro. We found that ABL-L-induced inhibition of cell proliferation was associated with an increase in G1-phase arrest. Typical apoptotic morphological and biochemical features were also observed in treated cells. Furthermore, the levels of the anti-apoptotic Bcl-2, pro-caspase 3/8/9 and poly(ADP-ribose) polymerase PARP decreased, and the level of pro-apoptotic Bax increased. Involvement of the caspase-mediated apoptosis was confirmed using caspase inhibitor Z-VAD-FMK pretreatment. In addition, ABL-L induced a tumor suppressor p53 and its target genes expression p21, fas, noxa and puma. The results of p53 knockdown suggest that caspase-mediated apoptosis induced by ABL-L was in p53-dependent pathway on HEp-2 cells. Our data indicate that the cytotoxicity of the novel semisynthetic analogue ABL-L involved G1 cell cycle arrest and apoptosis via a p53-dependent, caspase-mediated pathway on human laryngocarcinoma cells. [ABSTRACT FROM AUTHOR]

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Background: Laryngeal cancer (LC) remains one of the most common tumors of the respiratory tract, the exact pathogenesis remains unclear. MiRNA-106a-5p is aberrantly expressed in a variety of cancers and plays a pro- or anti-cancer role, but is indistinct in LC., Objectives: Showing the role of miRNA-106a-5p in the development of LC., Materials and Methods: Quantitative reverse transcription-polymerase chain reaction was used for miR-106a-5p measurement in clinical samples and LC cell lines (AMC-HN8 and TU212), first. The expression of miR-106a-5p was inhibited by inhibitor, then followed clonogenic and flow cytometric assays for cell proliferation; wood healing, and Transwell assays for cell migration. Dual luciferase reporter assay was performed for interaction verification, and the activation of the signal pathway was detected by western blots., Results: MiR-106a-5p was significantly over-expressed in LC tissues and cell lines. The proliferation ability of the LC cells was significantly reduced after miR-106a-5p inhibition, and most LC cells were stagnated in the G1 phase. The migration and invasion ability of the LC cells was decreased after the miR-106a-5p knockdown. Further, we found that miR-106-5a is bound with 3'-UTR of AKT interacting protein ( AKTIP ) mRNA specifically, and then activate PI3K/AKT/m-TOR pathway in LC cells., Conclusions: A new mechanism was uncovered that miR-106a-5p promotes LC development via AKTIP/PI3K/AKT/m-TOR axis, which guides clinical management and drug discovery., Competing Interests: All authors have completed the ICMJE uniform dis- closure form. The authors have no conflicts of interest to declare., (Copyright: © 2021 The Author(s); Published by Iranian Journal of Biotechnology.)

Objective: To research the efficacy of partial laryngectomy combined with sinupret drugs on patients with laryngocarcinoma. Methods: 102 cases of patients with laryngocarcinoma who were treated with PL surgery in our hospital from March2008 to March 2013 were chosen and randomly divided into observation group(51 cases) and control group(51 cases). The control group received antibiotics and nasal feeding, inhalation therapy and other programs, while the observation group was treated with sinupret drugs besides treatment of the control group. The clinical efficacy and postoperative pulmonary infection after 10 days of treatment were compared, and after six months of follow-up, the acoustic parameters were compared. Results: The effect of the observation group was significantly higher than that of control group, and the difference was statistically significant(P<0.05). The difference in Jitter, shimmer and normalized noise value(NNE) between observation group and control group were not statistically significant(P> 0.05). There were 5 cases of pulmonary infection in the observation group, which accounted for 9.80%, and was significantly lower than that in the control group(15 cases, accounting for 29.41%)(P<0.05). Conclusion: PL operation combined with Sinupret is effective in treatment of laryngeal cancer patients, can reduce pulmonary infection, and is worthy of recommendation. [ABSTRACT FROM AUTHOR]

Laryngocarcinoma is one of the most aggressive cancers that affects the head and neck region. The survival rate of patients with laryngocarcinoma is low due to late metastases and the resistance of the disease to chemotherapy and radiotherapy. Liriodenine, an alkaloid extracted from a number of plant species, has demonstrated antitumor effects on multiple types of cancer. However, the effects of liriodenine upon laryngocarcinoma, and the underlying mechanisms, are yet to be elucidated. The present study therefore investigated the potential antitumor effects of liriodenine on HEp-2 human laryngocarcinoma cells in vitro and HEp-2-implanted nude mice in vivo. Liriodenine induced significant apoptosis and inhibition of cell migration in the HEp-2 cells. Furthermore, the rate of tumor growth in the HEp-2-implanted nude mice was inhibited by the administration of liriodenine. The potential mechanism underlying the antitumor effects of liriodenine may result from an upregulative effect upon p53 expression, which ultimately induces cellular apoptosis. By contrast, the downregulation of p53 significantly reduced the antitumor effects of liriodenine. Together, these results suggest that liriodenine exhibits potent antitumor activities in laryngocarcinoma HEp-2 cells, in vitro and in vivo, via the upregulation of p53 expression. Liriodenine may therefore be a potential therapy for the treatment of laryngocarcinoma. [ABSTRACT FROM AUTHOR]

Testes-specific protease 50 (TSP50) is a potential cancer-associated gene that may be involved in human laryngocarcinoma. The present study aimed to investigate suppressive effects on the HEp2 human laryngocarcinoma cell line by transfection with TSP50-specific short hairpin RNA (shRNA). Western blot analysis was used to detect the expression levels of TSP50. MTT assay was used to evaluate cell proliferation. Wound healing was used in cell migration and invasion assays to evaluate the cell exercise capacity. Nuclear staining assay was used to evaluate cell apoptosis after knockdown of TSP50. Expression levels of TSP50 protein in the shRNA group were downregulated successfully by transfection, and the knockdown of endogenous TSP50 in HEp2 cells greatly inhibited nuclear factor κB (NF-κB) activity. MTT results showed that the cell proliferation in the shRNA group was significantly more depressed than that in the blank ( P < 0.05) and negative control groups ( P < 0.05). Additionally, a decreased number of migrated cells in the shRNA group was observed ( P < 0.05) using a cell migration and invasion assay. Moreover, knockdown of endogenous TSP50 expression can induce apoptosis in HEp2 Cells. These data indicated that knockdown of TSP50 may cause inhibition of proliferation, migration, and invasion of HEp2 cells. This study provides a new perspective in understanding the molecular mechanisms underlying the progression of laryngocarcinoma and offers a potential therapeutic target for laryngocarcinoma. [ABSTRACT FROM AUTHOR]

Abstract: In our previous study, a potential antitumor polysaccharide (LSPc1) was screened from the fruiting bodies of Lepista sordida. However, its molecular mechanism of cell death induction on Hep-2 human laryngocarcinoma cells has still not been determined. The present study evaluated the anticancer efficacy and associated mechanisms of LSPc1 on Hep-2 cells in vitro. We found that LSPc1-induced inhibition of cell proliferation was associated with an increase in G2/M-phase arrest at 48h. Typical morphological and biochemical features of apoptosis were also observed in LSPc1-treated cells. Furthermore, LSPc1 led a loss of mitochondrial membrane potential (ΔΨm), increased the ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2, induced cytochrome c release, and increased the activity of caspase-3 and -9, which altogether account for apoptotic cell death. Taken together, our study suggests that intrinsic mitochondrial caspase dependent pathway plays a very important role in LSPc1-induced cancer apoptosis and these results provided strong experimental evidence for the use of LSPc1 as a potential therapeutic agent in cancer for laryngocarcinoma. [Copyright &y& Elsevier]

Highlights: [•] Four polysaccharides (LSPa1, LSPb1, LSPb2 and LSPc1) were purified from Lepista sordida. [•] LSPb1, LSPb2 and LSPc1 exhibited more potent in vitro antitumor effect than LSPa1. [•] LSPc1 evidently suppressed the tumor growth in mice bearing human laryngocarcinoma Hep-2 cells. [•] The various physicochemical properties resulted in the difference of antitumor activity of four polysaccharides. [Copyright &y& Elsevier]

Background: LINC00941 has been proved to be related to various tumors, but its relationship with laryngocarcinoma remains vague., Methods: LINC00941 expression in laryngocarcinoma tumor and laryngocarcinoma cells was determined by real time-quantitative polymerase chain reaction (RT-qPCR). Besides, the five-year survival of laryngocarcinoma patients with different LINC00941 expression was analyzed with Kaplan-Meier survival analysis, and the clinical characteristics of laryngocarcinoma patients were also recorded. After transfection, cell viability, cell proliferation, apoptosis, cell cycle, migration, and invasion were detected by cell counting kit-8 (CCK-8), colony formation, flow cytometry, cell scratch, and Transwell assays, respectively. Glycolysis was assessed by the colorimetric method. Expressions of proliferation-associated proteins, migration-associated proteins, glycolysis-associated proteins, and phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signal pathway-associated proteins were detected by Western blot., Results: In laryngocarcinoma tumor tissues and cells, LINC00941 was highly expressed. High expression of LINC00941 decreased the 5-year survival of laryngocarcinoma patients, and it was positively related to lymph node metastasis and clinical stages. LINC00941 overexpression decreased apoptosis but promoted cell viability, proliferation, cell-cycle progression, migration, and invasion, and glucose consumption and lactate production in laryngocarcinoma cells. Moreover, LINC00941 overexpression elevated expressions of Ki-67, PCNA, MMP2, N-Cadherin, HK2, PFKFB4, and PKM, activated the PI3K/AKT/mTOR signal pathway but reduced E-Cadherin expression, while LINC00941 silencing had the opposite effects. PKM overexpression reversed the effects of LINC00941 silencing on cellular and glycolytic phenotypes., Conclusion: LINC00941 promoted in vitro progression and glycolysis of laryngocarcinoma cells by upregulating PKM via activating the PI3K/AKT/mTOR signaling pathway., (© 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.)

In recent years, the incidence of laryngeal carcinoma has been on the increase. The aim of the present study was to examine the expression level of endothelin-1 (ET-1) in laryngeal carcinoma tissues and to establish its clinical significance. A total of 82 cases of laryngeal carcinoma tissues were examined, of which 27 cases were stage I, 34 were stage II, and 21 were stage III. The normal mucosal tissues beyond the surgical incision margin in the 82 laryngeal carcinoma patients were used as the normal control. An additional 80 tissue specimens collected from laryngeal carcinoma outpatients were used as benign lesions. ET-1 expression levels in different tissues were determined using streptavidin-peroxidase (SP) immunohistochemistry. The results showed that the ET-1 expression level was highest in laryngeal carcinoma tissues and was significantly higher than that in the other two groups (P<0.05). The ET-1 expression level was higher in stage III compared to that in stage I and II (P<0.05) and higher than that of the normal control (P<0.05). The ET-1 expression level was higher in stage II compared to that in stage I (P<0.05). In conclusion, ET-1 was strongly expressed in laryngeal carcinoma tissues and may play an important role in the pathogenesis and development of laryngeal carcinoma tissues. ET-1 expression in laryngeal carcinoma tissues was associated with the clinical staging of laryngeal carcinoma. [ABSTRACT FROM AUTHOR]

Glucose Transporter-1 (GLUT-1) is considered to be a possible intrinsic marker of hypoxia in malignant tumors, which is an important factor in radioresistance of laryngocarcinoma. We speculated that the inhibition of GLUT-1 expression might improve the radiosensitivity of laryngocarcinoma. GLUT-1 siRNA was designed to inhibit the GLUT-1 expression, but the high molecular weight and difficult drug delivery limited the application. Herein, we constructed a glycolipid polymer chitosan oligosaccharide grafted stearic acid (CSSA) to conjugate siRNA via electrostatic interaction. The characteristics of CSSA and CSSA/siRNA were studied, as well as the radiosensitization effect of siRNA on human laryngocarcinoma epithelial (Hep-2) cells. Compared with the traditional commercial vector LipofectamineTM2000 (Lipo), CSSA exhibited lower cytotoxicity, more efficiently cellular uptake. Incubating with CSSA/siRNA, the survival rates of Hep-2 cells were significantly decreased comparing with either the group before transfection or Lipo/siRNA. CSSA is a promising carrier for efficient siRNA delivery and radiosensitization of laryngocarcinoma. [ABSTRACT FROM AUTHOR]