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Background Laryngeal cancer (LCA) is a common head and neck cancer. Lysine demethylase 5B (KDM5B) knockdown is expected as a new target for cancer prevention. We investigated the molecular mechanism of KDM5B in LCA. Materials and methods The levels of KDM5B, microRNA (miR)-139-3p and high-mobility-group box 2 (SOX2) in LCA tissues and cells, normal tissues and cells were detected. The effect of KDM5B on LCA was evaluated. The upstream miR of KDM5B and the downstream gene and pathway of KDM5B were predicted and their effects on LCA were analyzed. The Wnt/β-catenin pathway-specific activator agonist was delivered into LCA cells expressing miR-139-3p mimic to evaluate the role of the Wnt/β-catenin pathway. Results KDM5B was highly expressed in LCA, and inhibition of KDM5B suppressed LCA progression. miR-139-3p, downregulated in LCA tissues, was a regulatory miR of KDM5B. Overexpression of miR-139-3p significantly inhibited the malignant biological behaviors of LCA cells. KDM5B promoted SOX2 expression via histone demethylation. SOX2 was highly expressed in LCA, and overexpression of SOX2 promoted LCA progression by inducing the Wnt/β-catenin pathway. Activated Wnt/β-catenin pathway attenuated the inhibitory effect of miR-139-3p mimic on the malignant biological behaviors of LCA cells. Conclusion miR-139-3p overexpression inhibited LCA development via regulating the KDM5B/SOX2 axis and inhibiting the Wnt/β-catenin pathway.

Zili Chen,1,* Yifei Ma,2,* Yaozhen Pan,1 Shi Zuo,1 Haitao Zhu,1 Chao Yu,1 Changhao Zhu,1 Chengyi Sun1 1Department of Hepatobiliary Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, People’s Republic of China; 2Department of Otorhinolaryngology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, People’s Republic of China*These authors contributed equally to this workCorrespondence: Chengyi SunDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guizhou Medical University, No. Guiyi Street, Yunyan District, Guiyang, Guizhou 550004, People’s Republic of ChinaEmail chenyisun004@126.comBackground: Previous studies indicated that long noncoding RNAs (lncRNAs) played vital roles in the development and progression of hepatocellular carcinoma (HCC). Recently, downregulation of lncRNA RP5‑833A20.1 has been observed in HCC tissues. However, the underlying mechanism by which RP5‑833A20.1 regulates the proliferation and apoptosis in HCC has not been investigated. Thus, this study aimed to investigate the role of RP5‑833A20.1 in the progression of HCC.Methods: The levels of RP5‑833A20.1 in 30 pairs of HCC tissues and adjacent normal tissues were detected by RT-qPCR. In addition, the effects of RP5‑833A20.1 on cell proliferation, apoptosis and invasion were evaluated by CCK-8, flow cytometric, transwell assays, respectively. Meanwhile, the dual-luciferase reporter system assay was used to explore the interaction of RP5‑833A20.1 and miR-18a-5p in HCC.Results: The level of RP5‑833A20.1 was significantly downregulated in HCC tissues and HCC cell lines. Downregulation of RP5‑833A20.1 markedly promoted the proliferation and invasion of Bel-7402 cells. In addition, overexpression of RP5‑833A20.1 notably inhibited the proliferation and invasion of Huh7 cells. Moreover, overexpression of RP5‑833A20.1 obviously induced the apoptosis of Huh7 cells via increasing the levels of Bax and active caspase 3, and decreasing the levels of Bcl-2, p-Akt and p-ERK. Meanwhile, in vivo experiments performed also indicated that overexpression of RP5-833A20.1 could inhibit the tumorigenesis of subcutaneous Huh7 xenograft in nude mice. Furthermore, bioinformatics and luciferase reporter assay identified that RP5-833A20.1 functioned as a competing endogenous RNA (ceRNA) for miR-18a-5p in HCC.Conclusion: In this study, we found that RP5‑833A20.1 was downregulated in HCC tissues. In addition, RP5-833A20.1 could suppress the tumorigenesis in HCC through inhibiting Akt/ERK pathway by acting as a ceRNA for miR-18a-5p. Therefore, RP5-833A20.1 might be a valuable and potential biomarker and therapeutic target for the treatment of HCC.Keywords: hepatocellular carcinoma, long noncoding RNA RP5‑833A20.1, microRNA-18a-5p, proliferation

Background Previous studies indicated that long noncoding RNAs (lncRNAs) played vital roles in the development and progression of hepatocellular carcinoma (HCC). Recently, downregulation of lncRNA RP5‑833A20.1 has been observed in HCC tissues. However, the underlying mechanism by which RP5‑833A20.1 regulates the proliferation and apoptosis in HCC has not been investigated. Thus, this study aimed to investigate the role of RP5‑833A20.1 in the progression of HCC. Methods The levels of RP5‑833A20.1 in 30 pairs of HCC tissues and adjacent normal tissues were detected by RT-qPCR. In addition, the effects of RP5‑833A20.1 on cell proliferation, apoptosis and invasion were evaluated by CCK-8, flow cytometric, transwell assays, respectively. Meanwhile, the dual-luciferase reporter system assay was used to explore the interaction of RP5‑833A20.1 and miR-18a-5p in HCC. Results The level of RP5‑833A20.1 was significantly downregulated in HCC tissues and HCC cell lines. Downregulation of RP5‑833A20.1 markedly promoted the proliferation and invasion of Bel-7402 cells. In addition, overexpression of RP5‑833A20.1 notably inhibited the proliferation and invasion of Huh7 cells. Moreover, overexpression of RP5‑833A20.1 obviously induced the apoptosis of Huh7 cells via increasing the levels of Bax and active caspase 3, and decreasing the levels of Bcl-2, p-Akt and p-ERK. Meanwhile, in vivo experiments performed also indicated that overexpression of RP5-833A20.1 could inhibit the tumorigenesis of subcutaneous Huh7 xenograft in nude mice. Furthermore, bioinformatics and luciferase reporter assay identified that RP5-833A20.1 functioned as a competing endogenous RNA (ceRNA) for miR-18a-5p in HCC. Conclusion In this study, we found that RP5‑833A20.1 was downregulated in HCC tissues. In addition, RP5-833A20.1 could suppress the tumorigenesis in HCC through inhibiting Akt/ERK pathway by acting as a ceRNA for miR-18a-5p. Therefore, RP5-833A20.1 might be a valuable and potential biomarker and therapeutic target for the treatment of HCC.

BACKGROUND: By the time they are clinically diagnosed, patients with hepatocellular carcinoma (HCC) are often at the advanced stage. DNA methylation has become a useful predictor of prognosis for cancer patients. Research on DNA methylation as a biomarker for assessing the risk of occurrence in HCC patients is limited. The purpose of this study was to develop an efficient methylation site model for predicting survival in patients with HCC. METHODS: DNA methylation and gene expression profile data were extracted from The Cancer Genome Atlas (TCGA) database. Markers of DNA-methylated site in two subsets (the training subset and the test subset) were identified using a random survival forest algorithm and Cox proportional hazards regression. Then, Gene Ontology annotations were applied to investigate the functions of DNA methylation signatures. RESULTS: A total of 37 hub genes containing 713 methylated sites were identified among the differentially methylated genes (DMGs) and differentially expressed genes (DEGs). Finally, seven methylation sites (cg12824782, cg24871714, cg18683774, cg22796509, cg19450025, cg10474350, and cg06511917) were identified. In the training group and the test group, the area under the curve predicting the survival of patients with HCC was 0.750 and 0.742, respectively. The seven methylation sites signature could be used to divide the patients in the training group into high- and low-risk subgroups [overall survival (OS): 2.81 vs. 2.11 years; log-rank test, P

Yifei Ma,1,2,* Zili Chen,3,* Guodong Yu2 1School of Clinical Medicine, Guizhou Medical University, Guiyang 550004, Guizhou, People’s Republic of China; 2Department of Otorhinolaryngology, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou, People’s Republic of China; 3Department of Hepatobiliary Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou, People’s Republic of China*These authors contributed equally to this workCorrespondence: Guodong Yu Tel/Fax +86-851-86855119Email GuodongYU453@163.comBackground: Laryngeal cancer (LCA) is a common head and neck cancer. Lysine demethylase 5B (KDM5B) knockdown is expected as a new target for cancer prevention. We investigated the molecular mechanism of KDM5B in LCA.Materials and Methods: The levels of KDM5B, microRNA (miR)-139-3p and high-mobility-group box 2 (SOX2) in LCA tissues and cells, normal tissues and cells were detected. The effect of KDM5B on LCA was evaluated. The upstream miR of KDM5B and the downstream gene and pathway of KDM5B were predicted and their effects on LCA were analyzed. The Wnt/β-catenin pathway-specific activator agonist was delivered into LCA cells expressing miR-139-3p mimic to evaluate the role of the Wnt/β-catenin pathway.Results: KDM5B was highly expressed in LCA, and inhibition of KDM5B suppressed LCA progression. miR-139-3p, downregulated in LCA tissues, was a regulatory miR of KDM5B. Overexpression of miR-139-3p significantly inhibited the malignant biological behaviors of LCA cells. KDM5B promoted SOX2 expression via histone demethylation. SOX2 was highly expressed in LCA, and overexpression of SOX2 promoted LCA progression by inducing the Wnt/β-catenin pathway. Activated Wnt/β-catenin pathway attenuated the inhibitory effect of miR-139-3p mimic on the malignant biological behaviors of LCA cells.Conclusion: miR-139-3p overexpression inhibited LCA development via regulating the KDM5B/SOX2 axis and inhibiting the Wnt/β-catenin pathway.Keywords: laryngeal cancer, microRNA-139-3p, lysine demethylase 5B, high-mobility-group box 2, Wnt/β-catenin pathway

There are problems such as high error rate and low efficiency if the quality of LED chip welding is manually inspected. Digital image processing is used in this paper to inspect the quality of LED chip welding. Due to the limited field of view and insufficient resolution of the X-ray camera, multiple acquisitions shall be made, so there is inevitably overlap between images. Based on characteristics of the parts to be inspected, a feature-based automatic locating method is proposed. The copper rods whose gray level are the lowest is chosen as featured. At first, features are extracted through threshold segmentation. Then, the geometric relation-ship of the features is used to locate LED parts in the image and the overlap is removed. After the locating of LED parts, the LED chips on the part can be further located and inspected and inspected. The algorithm is efficient, the locating of 161 part can be finished in less then one second. The time for locating and inspection of the 161 part is about 12.4 seconds.