Dataset Information

MiR-642 serves as a tumor suppressor in hepatocellular carcinoma by regulating SEMA4C and p38 MAPK signaling pathway.

ABSTRACT: Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence and high risk. Study of the role and mechanism of miRNAs are a hot spot of research providing new treatment ideas in malignant tumors. The effect of miR-642a on HCC progression and the underlying molecular mechanism were investigated. Expression of miR-642a and SEMA4C was measured by western blot analysis and RT-PCR. miR-642a expression was elevated while SEMA4C expression was attenuated in HCC tissues and cells. Results of luciferase reporter and western blot analyses show that miR-642a modulated SEMA4C expression by binding to its 3'UTR. Moreover, miR-642a negatively regulated SEMA4C expression. HCC cell migration and invasion was tested by Transwell assays. The findings revealed that the number of migrated and invaded cells were reduced by miR-642a mimic and raised by miR-642a inhibitor, indicating that miR-642a showed a suppression effect on HCC cell migration and invasion. Additionally, the migration and invasion of HCC cells were inhibited by SEMA4C siRNA, and SEMA4C reversed miR-642a effect on HCC migration and invasion. Furthermore, p38 MAPK signaling pathway was proven to be inhibited by miR-642a mimic, whereas facilitated by miR-642a inhibitor and SEMA4C siRNA could overturn the promotion effect of miR-642a inhibitor. Briefly, miR-642a targeted SEMA4C to repress HCC cell migration and invasion through p38 MAPK signaling pathway providing a new strategy for treatment of HCC patients.

SUBMITTER: Yu Z

PROVIDER: S-EPMC7436928 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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miR-642 serves as a tumor suppressor in hepatocellular carcinoma by regulating SEMA4C and p38 MAPK signaling pathway.

Yu Zaijun Z Du Yuehe Y Li Hongying H Huang Jichao J Jiang Deqing D Fan Jilong J Shen Yuelan Y Zhang Lingling L Yu Xiujuan X Xu Na N Ke Qungang Q

Oncology letters 20200730 4

Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence and high risk. Study of the role and mechanism of miRNAs are a hot spot of research providing new treatment ideas in malignant tumors. The effect of miR-642a on HCC progression and the underlying molecular mechanism were investigated. Expression of miR-642a and SEMA4C was measured by western blot analysis and RT-PCR. miR-642a expression was elevated while SEMA4C expression was attenuated in HCC tissues and cells. Results of ...[more]

PMID: 32863907

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Project description:Background:Nasopharyngeal carcinoma (NPC) is a common epithelial carcinoma with high occurrence and metastatic rates in Southern China. To date, the molecular mechanisms of metastasis for NPC remains unclear. The aim of this study was to discover the underlying mechanism of NPC and to elucidate novel genes that may play important roles in NPC progression and metastasis. Methods:We carry out mRNA expression profiling, Arraystar Human mRNA Expression Profiling Service Report based on polymerase chain reaction (PCR) using four pairs of tumor tissues and their corresponding benign adjacent tissues from NPC patients. Results:We found that 1,787 genes were differentially expressed, among them, 8 genes were identified as highly upregulated in NPC patients. Within these 8 genes, only TSPAN8 was consistently over-expressed in poorly differentiated CNE2 cell line and highly-metastatic subclone S18 cell line. TSPAN8 mRNA and protein levels were increased in primary carcinoma tissues compared to their corresponding adjacent benign tissues. Knockdown of TSPAN8 by siRNA resulted in inhibition of NPC cell migration and invasion, while overexpression of TSPAN8 promoted NPC cell migration, invasion and proliferation. To explore the potential metastasis pathway mechanism for NPC, TSPAN8 were silenced in CNE2 cell. From the Tumor Metastasis Pathway Finder PCR array, knockdown of TSPAN8 led to the down-regulation of IL-1?, which showed the most down-regulation among identified genes. IL-1? is a regulating factor of the Akt/MAPK pathway, which is involved in the cancer cell migration regulation. Furthermore, the down-regulation of TSPAN8 in CNE2 cell was associated with inhibition of the Akt/MAPK pathway. Immunohistochemistry (IHC) indicated that TSPAN8 level was increased in NPC tumors, which was associated with shorter overall survival and metastasis free survival (MFS). Conclusions:The data indicated that TSPAN8 acting as a tumor migration marker and may be a prognostic factor or therapeutic target for NPC.

Dataset Information

MiR-642 serves as a tumor suppressor in hepatocellular carcinoma by regulating SEMA4C and p38 MAPK signaling pathway.

Publications

miR-642 serves as a tumor suppressor in hepatocellular carcinoma by regulating SEMA4C and p38 MAPK signaling pathway.

Similar Datasets

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