The Mechanism Study Of LncRNA PTENP1/miR-3658/LASS2 Regulatory Axis In Bladder Cancer

Objective:In this study,a series of in vitro cell experiments were conducted to study the effects of lnc RNA PTENP1/miR-3658/LASS2 regulatory axis on the proliferation,apoptosis,migration,cell cycle and cisplatin chemotherapy sensitivity of bladder cancer cells,and to elaborate the possible molecular mechanism of this regulatory axis in the progression of bladder cancer.To identify potential tumor markers and novel targets for early diagnosis and treatment of bladder cancer.Methods:1.ln CAR,Lnc Locator and i Loc-Lnc RNA databases were used to analyze the secondary structure,protein coding potential and subcellular localization of PTENP1.2.The expression of PTENP1 in bladder cancer cell lines and clinical specimens was detected by q RT-PCR;The methylation status of PTENP1 in bladder cancer cell lines was detected by MSP.ISH was used to detect PTENP1 expression in bladder cancer.3.T24 cells and J82 cells were used to construct overexpressed/interfered PTENP1 cell models,and a series of cell function experiments were conducted to explore the effects of PTENP1 on proliferation,apoptosis,migration,cell cycle and cisplatin chemotherapy sensitivity of bladder cancer cells.4.The expression levels of miRNA-3658 and LASS2 after overexpression of PTENP1 were detected by q RT-PCR and Western blotting.5.The co-transfected miRNA-3658 cell model was constructed,and the effects of co-transfected miRNA-3658 on the proliferation,apoptosis,migration ability and cell cycle of bladder cancer cells were investigated through a series of cell function experiments.6.The expression level of LASS2 after co-transfection with miRNA-3658 was detected by q RT-PCR.Results:1.PTENP1 has only one secondary structure,and the transcript of PTENP1 has no protein coding potential and is strongly conserved,and it is mainly located in the cytoplasm.2.PTENP1 is significantly underexpressed in both bladder cancer cell lines and bladder cancer tissues,and the mechanism may be related to promoter methylation.3.In vitro experiments,overexpression of PTENP1 inhibited the proliferation and migration of T24 cells,kept the cell cycle at G0/G1 phase,promoted apoptosis,and increased the cisplatin sensitivity of bladder cancer cells.The reverse is true when PTENP1 is struck low.4.After overexpression of PTENP1,the expression of miR-3658 decreased and the expression of LASS2 increased in bladder cancer cells.After PTENP1 knockdown,the expression of miR-3658 increased and LASS2 decreased in bladder cancer cells.5.Co-transfection of miR-3658 mimics promoted the proliferation and migration of T24 cells,shortened the G0/G1 phase of tumor cells,and inhibited cell apoptosis;Co-transfection of miR-3658 inhibit the opposite.6.LASS2 expression decreased after co-transfection of miR-3658 mimics;After co-transfection with miR-3658 inhibit 2 expression increased.Conclusions:In bladder cancer,PTENP1 expression is down-regulated.In vitro,PTENP1 can inhibit the proliferation and migration of bladder cancer cells,promote cell apoptosis,cell cycle arrest,and increase cisplatin sensitivity,thus playing a role in cancer inhibition.Its possible mechanism of action is to inhibit the occurrence and development of bladder cancer through the miR-3658/LASS2 axis.This study conducted a preliminary study on the relationship between the regulatory axis of lnc RNA PTENP1/miR-3658/LASS2 and the malignant biological behavior and chemotherapy sensitivity of bladder cancer cells,which is expected to provide new ideas for the early diagnosis and treatment of bladder cancer.