Search

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。)

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.

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.

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]

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]

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 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]

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]

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.

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.)

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]

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]

Long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is abnormally expressed in numerous tumors and functions as an oncogene, but the role of NEAT1 in laryngocarcinoma is largely unknown. Our study validated that NEAT1 expression was markedly upregulated in laryngocarcinoma tissues and cells. Downregulation of NEAT1 dramatically suppressed cell proliferation and invasion through inhibiting miR-524-5p expression. Additionally, NEAT1 overexpression promoted cell growth and metastasis, while overexpression of miR-524-5p could reverse the effect. NEAT1 increased the expression of histone deacetylase 1 gene (HDAC1) via sponging miR-524-5p. Mechanistically, overexpression of HDAC1 recovered the cancer-inhibiting effects of miR-524-5p mimic or NEAT1 silence by deacetylation of tensin homolog deleted on chromosome ten (PTEN) and inhibiting AKT signal pathway. Moreover, in vivo experiments indicated that silence of NEAT1 signally suppressed tumor growth. Taken together, knockdown of NEAT1 suppressed laryngocarcinoma cell growth and metastasis by miR-524-5p/HDAC1/PTEN/AKT signal pathway, which provided a potential therapeutic target for laryngocarcinoma.

The effects of methylation/autophagy-related genes (MARGs) and immune infiltration in the tumor microenvironment on the prognosis of laryngeal cancer were comprehensively explored in this study. Survival analysis screened out 126 MARGs and 10 immune cells potentially associated with the prognosis of laryngeal carcinoma. Cox and lasso regression analyses were then used to select 8 MARGs (CAPN10, DAPK2, MBTPS2, ST13, CFLAR, FADD, PEX14 and TSC2) and 2 immune cells (Eosinophil and Mast cell) to obtain the prognostic risk scoring system (pRS). The pRS was used to establish a risk prediction model for the prognosis of laryngeal cancer. The predictive ability of the prediction model was evaluated by GEO datasets and our clinical samples. Further analysis revealed that pRS is highly associated with single nucleotide polymorphism (SNP), copy number variation (CNV), immune checkpoint blockade (ICB) therapy and tumor microenvironment. Moreover, the screened pRS-related ceRNA network and circ&#95;0002951/miR-548k/HAS2 pathway provide potential therapeutic targets and biomarkers of laryngocarcinoma. Based on the clustering results of pRS-related genes, single cells were then genotyped and revealed by integrated scRNA-seq in laryngeal cancer samples. Fibroblasts were found enriched in high risk cell clusters at the scRNA-seq level. Fibroblast-related ligand-receptor interactions were then exposed and a neural network-based deep learning model based on these pRS-related hub gene signatures was also established with a high accuracy in cell type prediction. In conclusion, the combination of single-cell and transcriptome laryngeal carcinoma landscape analyses can investigate the link between the tumor microenvironmental and prognostic characteristics., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

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., Competing Interests: Conflict of interest The authors declare that there is no conflict of interest., (Copyright © 2021 Zong et al. Published by Tehran University of Medical Sciences.)

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., (Copyright © 2020 American Society for Microbiology.)

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.

Mediator 19 (Med19) is a component of the mediator complex which is a co-activator for DNA-binding factors that activate transcription via RNA polymerase II. Accumulating evidence has shown that Med19 plays important roles in cancer cell proliferation and tumorigenesis. The physiological mechanism by which Med19 exerts its promoting effects in laryngocarcinoma is not yet fully understood. Here, we found that the expression of Med19 was increased in laryngocarcinoma samples from patients compared to normal bone tissues. Med19 knockdown significantly induced growth inhibition and suppressed migration in the HEp2 cell lines. Med19 knockdown also induced apoptosis in HEp2 cells via activation of caspase-3, 9 and Apaf-1. In addition, The tumorigenicity of Med19 short hairpin RNA (shRNA)-expressing cells were decreased after inoculating into nude mice. Taken together, our data suggest that Med19 acts as an oncogene in laryngocarcinoma via a possible caspase modulation pathway.

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.

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.