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• W2891363685 abstract "Long non-coding RNA-metastasis-associated lung adenocarcinoma transcript (LncR-MALAT) is highly expressed in a variety of tumors, which can affect the progression of tumor cells. LncR-MALAT1 was reported to affect the proliferation of pancreatic cancer and glioma cells by regulating autophagy, but how LncR-MALAT1 affects the proliferation and invasion of various cancer cells by regulating autophagy in bladder cancer has not been reported. Therefore, in this study, we aimed to investigate the effect of LncR-MALAT1 on cell proliferation, apoptosis, invasion and autophagy of bladder cancer and the possible mechanism in vitro. The results showed that LncR-MALAT1 was highly expressed in bladder cancer tissues and cells. The silence of LncR-MALAT1 inhibited the proliferation and invasion and promoted apoptosis in bladder cancer cells. In addition, MALAT1 shRNA down-regulated the expression of Beclin1 and the LC3 II/I ratio, enhanced the expression of p62 and played a significant role in autophagy inhibition. By further investigating the relevant regulatory mechanisms, we found that MALATI shRNA reduced the phosphorylation of AMPK and increased the phosphorylation level of mTOR, thereby inhibiting the activation of the AMPK/mTOR pathway. It is noteworthy that the AMPK/mTOR pathway activator, metformin, partially reversed the effect of MALAT1 shRNA on the inhibition of autophagy in bladder cancer cells. At the same time, the proliferation and invasion ability of HT-1376 cells inhibited by MALAT1 shRNA were also enhanced. The results showed that down-regulation of LncR-MALAT1 could inhibit the proliferation and invasion of bladder cancer cells by attenuating autophagy via the regulation of the AMPK/mTOR pathway." @default.
• W2891363685 created "2018-09-27" @default.
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• W2891363685 date "2018-01-01" @default.
• W2891363685 modified "2023-09-27" @default.
• W2891363685 title "Down-regulated LncR-MALAT1 suppressed cell proliferation and migration by inactivating autophagy in bladder cancer" @default.
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• W2891363685 doi "https://doi.org/10.1039/c8ra04876b" @default.
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