MiR-16-5p Promotes the Progression of Esophageal Squamous Cell Carcinoma via Regulating AMPK/mTOR Signaling Pathway.

IF 1.1 4区医学 Q4 MEDICAL LABORATORY TECHNOLOGY

Annals of clinical and laboratory science Pub Date : 2024-09-01

Wen-Xiu Yu, Min Zhou, Zhi-Jing Yin, Na Ji, Hai-Lin Yu

{"title":"MiR-16-5p Promotes the Progression of Esophageal Squamous Cell Carcinoma via Regulating AMPK/mTOR Signaling Pathway.","authors":"Wen-Xiu Yu, Min Zhou, Zhi-Jing Yin, Na Ji, Hai-Lin Yu","doi":"","DOIUrl":null,"url":null,"abstract":"Objective: Esophageal squamous cell carcinoma (ESCC) is commonly diagnosed with high mortality worldwide. Cell proliferation and cell apoptosis are essential biological processes for the development of cancers. MiR-16-5p, a critical member of miRNAs family, is involved in cell apoptosis and tumor progression. However, the role of miR-16-5p in regulating esophageal squamous cell carcinoma and the underlying mechanism remain unclear.Methods: In this study, we used human ESCC tissue samples and human esophageal cells to determine the expression level of miR-16-5p in ESCC tissues and cells. Cell Counting Kit-8 assay and flow cytometry were used to test cell proliferation and apoptosis. Western blotting was used to detect protein expression levels. The scratch assay was used to analyze the level of cell migration, and the transwell assay was used to analyze the invasive ability of tumor cells.Results: The expression of miR-16-5p was up-regulated in ESCC tissues and cells. Knockdown of miR-16-5p significantly inhibited cell proliferation and promoted cell apoptosis. The knockdown of miR-16-5p also restrained cell migration and invasion. We revealed that AMPK/mTOR signaling pathway participated in the regulation of ESCC progression.Conclusion: miR-16-5p may promote the proliferation, migration, and invasion of ESCC through modulating AMPK/mTOR signaling pathway.","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"54 5","pages":"569-576"},"PeriodicalIF":1.1000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of clinical and laboratory science","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICAL LABORATORY TECHNOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Objective: Esophageal squamous cell carcinoma (ESCC) is commonly diagnosed with high mortality worldwide. Cell proliferation and cell apoptosis are essential biological processes for the development of cancers. MiR-16-5p, a critical member of miRNAs family, is involved in cell apoptosis and tumor progression. However, the role of miR-16-5p in regulating esophageal squamous cell carcinoma and the underlying mechanism remain unclear.

Methods: In this study, we used human ESCC tissue samples and human esophageal cells to determine the expression level of miR-16-5p in ESCC tissues and cells. Cell Counting Kit-8 assay and flow cytometry were used to test cell proliferation and apoptosis. Western blotting was used to detect protein expression levels. The scratch assay was used to analyze the level of cell migration, and the transwell assay was used to analyze the invasive ability of tumor cells.

Results: The expression of miR-16-5p was up-regulated in ESCC tissues and cells. Knockdown of miR-16-5p significantly inhibited cell proliferation and promoted cell apoptosis. The knockdown of miR-16-5p also restrained cell migration and invasion. We revealed that AMPK/mTOR signaling pathway participated in the regulation of ESCC progression.

Conclusion: miR-16-5p may promote the proliferation, migration, and invasion of ESCC through modulating AMPK/mTOR signaling pathway.

本刊更多论文

MiR-16-5p 通过调节 AMPK/mTOR 信号通路促进食管鳞状细胞癌的进展

目的：食管鳞状细胞癌（ESCC）是全球常见的高死亡率癌症。细胞增殖和细胞凋亡是癌症发生发展的重要生物学过程。miR-16-5p 是 miRNAs 家族的重要成员，参与细胞凋亡和肿瘤进展。然而，miR-16-5p 在调控食管鳞状细胞癌中的作用及其内在机制仍不清楚：本研究采用人类 ESCC 组织样本和人类食管细胞来测定 miR-16-5p 在 ESCC 组织和细胞中的表达水平。采用细胞计数试剂盒-8测定法和流式细胞术检测细胞增殖和凋亡。采用 Western 印迹法检测蛋白质表达水平。划痕试验用于分析细胞的迁移水平，透孔试验用于分析肿瘤细胞的侵袭能力：结果：miR-16-5p在ESCC组织和细胞中表达上调。结果：miR-16-5p 在 ESCC 组织和细胞中表达上调，敲除 miR-16-5p 能明显抑制细胞增殖并促进细胞凋亡。敲除 miR-16-5p 还能抑制细胞迁移和侵袭。结论：miR-16-5p 可通过调节 AMPK/mTOR 信号通路促进 ESCC 的增殖、迁移和侵袭。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Annals of clinical and laboratory science 医学-医学实验技术

CiteScore

1.60

自引率

0.00%

发文量

112

审稿时长

6-12 weeks

期刊介绍： The Annals of Clinical & Laboratory Science welcomes manuscripts that report research in clinical science, including pathology, clinical chemistry, biotechnology, molecular biology, cytogenetics, microbiology, immunology, hematology, transfusion medicine, organ and tissue transplantation, therapeutics, toxicology, and clinical informatics.