Jichu yixue yu linchuang (Jun 2022)

Down-regulation of lncRNA RHPN1-AS1 inhibits proliferation and migration of human bladder cancer cell line T24

  • BAI Bing, ZHANG Hai-fang, YANG Qing-liang, QIN Yue, ZHOU Chen-long, SONG Ge, WANG Ying

DOI
https://doi.org/10.16352/j.issn.1001-6325.2022.06.004
Journal volume & issue
Vol. 42, no. 6
pp. 940 – 944

Abstract

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Objective To explore the effect of interfering with lncRNA RHPN1-AS1 on the biological behavior of bladder cancer cell T24 and its mechanism. Methods RT-qPCR method was used to detect the expression of RHPN1-AS1 and miR-149-3p by bladder cancer tissues and adjacent tissues.si-NC,si-RHPN1-AS1, si-RHPN1-AS1,anti-miR-NC, si-RHPN1-AS1 and miR-149-3p inhibitor were transfected into bladder cancer cell T24. The expression of RHPN1-AS1 and miR-149-3p in T24 cells were examined by RT-qPCR.MTT, plate colony formation experiment, scratch experiment, flow cytometry were used to detect cell proliferation, migration ability and cell apoptosis rate respectively. The dual luciferase reporter experiment was used to detect the targeting relationship between RHPN1-AS1 and miR-149-3p. Bax and Bcl-2 protein expression was assessed using Western blot. Results Compared with adjacent tissues, the expression of RHPN1-AS1 in bladder cancer tissue was increased(P<0.05) and the expression of miR-149-3p was decreased (P<0.05). Compared with the si-NC group, transfection of si-RHPN1-AS1 significantly reduced cell proliferation, scratch healing rate and the protein level of Bcl-2(P<0.05), reduced the number of clones (P<0.05)and increased apoptosis rate and the protein level of Bax(P<0.05). Compared with the si-RHPN1-AS1+anti-miR-NC group, transfection of si-RHPN1-AS1 and miR-149-3p inhibitor significantly increased cell proliferation, scratch healing rate and the protein level of Bcl-2 (P<0.05) increased the number of clones formed (P<0.05), reduced the apoptosis rate and the protein level of Bax (P<0.05). Conclusions Interfering with the expression of RHPN1-AS1 may inhibit the proliferation and migration of bladder cancer cells and may promote cell apoptosis by up-regulating miR-149-3p.

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