Abstract
Objective To investigate the expression of long-stranded non-coding RNA HOXA transcript at the distal tip (HOTTIP) (lncRNA HOPTTIP) in bladder cancer cells (BCC) and its effect on proliferation, migration and invasion of BCC and potential mechanisms. Methods Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the expression differences of HOTTIP between normal tissue and bladder cancer tissues, normal cell and bladder cancer cell. Cell counting kit-8 (CCK-8) was used to observe the proliferation levels of BCC. Cell cycle progression of BCC was detected by flow cytometry. Cell invasion and metastasis were observed by transwell and wound healing experiments. Western blotting assay was used to detect the protein expressions of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase (TIMPs). Results The expression level of HOTTIP in BCC (1.943±0.251) was significantly higher than that of paracancerous tissue (1.002±0.091), and the difference was statistically significant (P<0.05); The expression of HOTTIP in human normal epithelial cells (SV-HUC-1) was significantly lower than that of 5637 and T24 (1.003±0.092 vs. 2.241±0.306 and 1.692±0.203), with significant difference (P<0.05). After si-HOTTIP and si-NC intervention 48h on 5637 and T24 cells, the proliferation of 5637 (0.881±0.182 vs. 1.824±0.193) and T24 (0.623±0.094 vs. 1.332±0.153) cells decreased significantly (P<0.05), the cell cycle were stuck into G0/G1 phase, rate of invasion and migration were reduced, MMP-2 and MMP-9 protein expression levels decreased, TIMP1 and TIMP2 protein expression levels increased. Conclusion Long-stranded non-coding RNA (LncRNA) HOTTIP is down-regulated in bladder cancer tissues and cells, and promotes the proliferation, migration and invasion of BCC by decreasing MMPs and increasing TIMPs. Key words: Long non-coding RNAHOXA transcript at the distal tip; Bladder cancer; Proliferation; Migration; Invasion
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