miR-204 regulates the EMT by targeting snai1 to suppress the invasion and migration of gastric cancer

Abstract

miR-204 was found to be downregulated in gastric cancer (GC) tissues, and the effect of miR-204 function on gastric cancer remains as a mystery. Therefore, this study was aimed at investigating the potential role of miR-204 involved in GC progression. Tissues collected from 60 gastric cancer patients were selected as the case group, while the matched normal paracancer tissues as controls. miR-204 expression levels in tissues and GC cells were detected using real-time fluorescent quantitative PCR. Luciferase assay was adopted to validate the interaction between potential gene targets and miR-204. Transwell assay was performed to evaluate the metastasis of GC cells. By building the epithelial-mesenchymal transition (EMT) model in vitro through the addition of transforming growth factor beta 1 (TGF-β1), expressions of miR-204 and snai1 in the EMT model together with their respective effects on EMT were evaluated. miR-204 was significantly downregulated in GC tissues and invasive GC cells (P < 0.05). The over-expression of miR-204 or downregulation of snai1 could significantly inhibit the metastasis and invasion of GC cells both in vitro and in vivo. The upregulated miR-204 expression or inhibited snai1 expression could suppress the EMT process in EMT in vitro models. Our study provided evidence that miR-204 may suppress the metastasis and invasion of GC cells through the regulation of the EMT process by targeting snai1.

Histological and Pathological Assessment of miR-204 and SOX4 Levels in Gastric Cancer Patients

“…In this study, we examined that miR-204 not only suppressed proliferation but also suppressed migration and invasion of gastric cancer cells. In other studies, Zhang et al, Zhang et al, and Liu et al also documented that miR-204 was a suppressor in gastric cancer, which supported our findings [11, 22, 23]. Therefore, miR-204 played a comprehensive suppressing role in many kinds of human cancers.…”

“…Previous studies showed that miR-204 suppressed gastric cancer through targeting USP47, RAB22A, SIRT1, Snai1, and so forth [11, 22, 23]. Getting together, in miR-204 regulation pathway, USP47, RAB22A, SIRT1, Snai1, and so forth and SOX4 may play an associating role contributing to gastric cancer progressing.…”

“…MiR-204 is one of the miRNAs that have been determined to suppress tumor initiation and development in lung cancer, esophageal cancer, gastric cancer, and other cancers [11, 20, 21]. USP47, RAB22A, SIRT1, Snai1, and so forth are targets of miR-204 that mediate miR-204 reducing the oncogenicity of gastric cancer [11, 22, 23]. But there was no fully histological and pathological research about miR-204 in gastric cancer patients in previous studies.…”

A Downmodulated MicroRNA Profiling in Patients with Gastric Cancer

“…A very recent review believes that miR-204 acts as a tumor suppressor via promoting apoptosis, decreasing resistance of cancer cells to chemotherapy, and suppressing the self-renewal of cancer stem cells [32]. Interestingly, several research groups tentatively documented the underlying mechanisms that how miR-204 functions in GC development [15, 24, 31, 33]. For example, Sacconi et al demonstrated that miR-204 targeted B cell lymphoma-2 (Bcl-2) mRNA and increased responsiveness of GC cells to 5-fluorouracil and oxaliplatin treatment, and ectopic expression of Bcl-2 counteracted miR-204 proapoptotic activity [15].…”

MicroRNA-214 promotes peritoneal metastasis through regulating PTEN negatively in gastric cancer

“…Notably, cell lines MKN-28NM and GC9811 had low metastatic potential to the peritoneum while GC9811-P and MKN-28M had higher metastatic potential [21,22]. Cells were grown in the medium of RPMI-1640 (HyClone, USA) containing 10% FBS (fetal bovine serum, HyClone) at 37 • C atmosphere with 5% CO 2 .…”