miR‑21 inhibits autophagy and promotes malignant development in the bladder cancer T24�cell line

Abstract

is reported to exhibit cancer-promoting activity in various types of cancer. It has been previously demonstrated that miR-21 is overexpressed in bladder tumor tissue compared with normal mucosa. However, the functional mechanism of miR-21 in bladder cancer remains largely unknown. Thus, the current study aimed to determine the roles of miR-21 in autophagy and the malignant development of bladder cancer in T24 cells. Upregulation or downregulation of miR-21 was achieved following the transfection of miR-21 mimic or miR-21 inhibitor. An MTT assay was additionally performed to measure cell growth. Wound healing and transwell invasion assays were used to detect cell migration and invasion. The apoptotic potential and cell cycle were examined via flow cytometry and reverse transcription-quantitative PCR was performed to evaluate the expression of phosphatase and tensin homolog (PTEN), beclin 1, microtubule-associated protein l light chain 3B (LC3-II), cyclin D1, caspase-3, E-cadherin, matrix metallopeptidase-9 (MMP-9) and vimentin. The results revealed that the proliferation, migration and invasion of T24 cells was greatly increased in the miR-21 mimic group, while apoptosis was greatly inhibited. Additionally, T24 cells treated with miR-21 mimic exhibited G1-phase arrest. In the miR-21 mimic group, the expression of PTEN, beclin 1, LC3-II, caspase-3 and E-cadherin were decreased, while the expression of cyclin D1, MMP-9 and vimentin were increased. Opposite effects were observed in the miR-21 inhibitor group. The data of the current study may indicate that miR-21 overexpression inhibited autophagy and promoted the proliferation, migration, invasion and epithelial to mesenchymal transition of bladder cancer T24 cells. The results may further elucidate the molecular mechanism of miR-21 in the development of bladder cancer. Materials and methodsCell line and culture. The human bladder cancer cell line, T24, was obtained from the Cell Bank of Type Culture Collection of the Chinese Academy of Sciences. Cells were cultured in

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