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MiR-17-5p Inhibits the Proliferation and Metastasis of Gastric Cancer Cells by Targeting PTEN Protein.

癌症 小RNA 转移 医学 癌细胞 癌症研究 PTEN公司 转染 肿瘤科 内科学 细胞培养 细胞凋亡 生物 基因 PI3K/AKT/mTOR通路 生物化学 遗传学
作者
Yifei Sun,Chun-Xiao Hu,Li Dinuo
出处
期刊:PubMed 卷期号:28 (8): 23-29 被引量:11
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摘要

Effectively inhibiting gastric-cancer metastasis and decreasing the recurrence of gastric cancer after surgery are urgent problems. In recent years, abnormal microRNA (miRNA) expression has been found in gastric cancer, and miRNA-17-5p has been found to regulate the occurrence and progression of various cancers. It's necessary to analyze miRNA-17-5p's action mechanism in gastric cancer.The study intended to investigate: (1) miR-17-5p expression in gastric-cancer tissues and adjacent normal tissues in clinical patients, (2) to explore the regulatory effects of miR-17-5p on the biological behavior of gastric cancer at the cellular level, by constructing a gastric-cancer cell model that uses overexpressing miR-17-5p, and (3) to discuss preliminarily its action mechanism.The research team designed a laboratory study.The study took place at the First Affiliated Hospital of Jinzhou Medical University in Jinzhou, Liaoning Province, China.Clinical specimens of gastric-cancer tissues and adjacent normal tissues were obtained from 20 patients who had undergone surgical resection for gastric cancer at the hospital.Quantitative reverse transcription (qRT)-polymerase chain reaction (PCR) was employed to detect miR-17-5p expression in the gastric-cancer tissues and cells. The si-miR-17-5p was transfected into gastric-cancer cell lines to establish a cell model, with the si-miR-17-5p becoming the intervention group and a negative control group, the si-NC group also being created. The cultured SGC-7901 cells were divided into miR-17-5p mimic group (si-miR-17-5p) and negative control group (si-NC) by transfecting si-miR-17-5p and transfection reagent Lipo2000 for research. Cell proliferation was detected using the cell counting kit-8 (CCK-8) assay; cell invasion and migration were measured using a Transwell assay; and cell migration was also measured using a wound-healing assay. A bioinformatics prediction, luciferase reporter gene assay, and western blot assay were applied to verify the downstream target protein of miR-17-5p.The miR-17-5p levels were significantly higher in gastric-cancer tissues and cell lines than in adjacent normal tissues or gastric epithelial cells. Gastric-cancer cells that were transfected with si-miR-17-5p were found to have significantly inhibited cell proliferation. The si-miR-17-5p could significantly suppress the invasion and metastasis of gastric-cancer cells. A bioinformatics prediction concluded that phosphatase and tensin homolog (PTEN) was the downstream target protein of miR-17-5p, which was confirmed by the Luciferase reporter gene assay and Western blot assay.The miR-17-5p was upregulated in gastric-cancer patients. Simultaneously, si-miR-17-5p dramatically inhibited the proliferation, invasion, and metastasis of gastric-cancer cells, and PTEN protein was its downstream target protein. The study provides a new approach to the treatment of gastric cancer.

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