Abstract
MicroRNAs (miRNAs) operate as tumor suppressor or carcinogen to regulate cell proliferation, metastasis, invasion, differentiation, apoptosis, and metabolic process. In the present research, we investigated the effect and mechanism of miR-496 in human gastric cancer cells. miR-496 was downregulated in two gastric cancer cell lines, AGS and MKN45, compared with normal gastric epithelial cell line GES-1. miR-496 mimics inhibited the proliferation of AGS cells after the transfection for 48 and 72 h. The migration and invasion of AGS cells were also inhibited by the transfection of miR-496 mimics. miR-496 mimics induced the apoptosis through upregulating the levels of Bax and Active Caspase 3 and downregulating the levels of Bcl-2 and Total Caspase 3. Bioinformatics analysis showed that there was a binding site between miR-496 and Lyn kinase (LYN). miR-496 mimics could inhibit the expression of LYN in AGS cells. LYN overexpression blocked the inhibition of tumor cell growth, as well as the inhibition of AKT/mTOR signaling pathway induced by miR-496. In conclusion, miR-496 inhibited the proliferation through the AKT/mTOR signaling pathway via targeting LYN in gastric cancer cells. Our research provides a new potential target for clinical diagnosis and targeted treatment for gastric cancer.
Highlights
MicroRNAs operate as tumor suppressor or carcinogen to regulate cell proliferation, metastasis, invasion, differentiation, apoptosis, and metabolic process
The role of miR-496 in human tumors has been gradually revealed. lncRNA DANCR was found to be involved in the progression of lung cancer through sponging miR-496 and regulating the level of mTOR [10]. miR496 can suppress gene expression and the proliferation in breast cancer cell lines MCF-10A, MCF-7, and MDA-MB231 [14]
We found that miR-496 was downregulated in AGS and MKN45 compared with the normal gastric epithelial cell line GES-1
Summary
This work is licensed under the Creative Commons Attribution 4.0 International miR-496 inhibits gastric cancer 1207. DMEM with 10% FBS was used for cell culture. MiR-496 mimics, miRNA mimics negative control, and Lyn kinase (LYN) overexpression plasmid were purchased from GenePharma (Shanghai, China) and transfected into AGS cells using Lipofectamine 2000 (Invitrogen, CA, USA) according to the manufacturer’s protocol. Cell viability was represented by OD value at 450 nm
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