RETRACTED: Exosome-derived PTENP1 suppresses cisplatin resistance of bladder cancer (BC) by suppressing cell proliferation, migration and inducing apoptosis via the miR-103a/PDCD4 axis (Retracted article. See vol. 11, pg. 6254, 2021)

被引:2
作者
Lu, Xingre [1 ]
Chen, Fengyu [1 ]
Yuan, Diao [1 ]
He, Xiang [1 ]
Liu, Xiaowen [1 ]
Zi, Yunju [1 ]
Lu, Yu [1 ]
机构
[1] Peoples Hosp Wenshan Prefecture Yunnan Prov, Dept Clin Lab, 228 Kaihua Middle Rd, Wenshan 663000, Yunnan, Peoples R China
关键词
RNA; EXPRESSION; CARCINOMA; INCREASES; MIR-19B; INHIBIT;
D O I
10.1039/c9ra07823a
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
Bladder cancer (BC) is a lethal cancer that threatens the health of millions of people. Chemotherapy drug resistance, for example, cisplatin (DDP) resistance, is a huge limitation for BC therapy. PTEN pseudogene-1 (PTENP1) has been identified as a significant biomarker of multiple cancers. Therefore, it is essential to illuminate the molecular mechanism of PTENP1 in BC cell DDP resistance and progression. Serum exosomes were isolated using an ExoQuick precipitation kit. Serum exosomes were round-shaped vesicles of 100 +/- 60 nm in size. The expression of PTENP1 was down-regulated in serum exosomes isolated from cisplatin non-responsive patients compared with responsive patients. ROC curves certified the diagnostic value of PTENP1. Apparently, PTENP1 transfection inhibited DDP-resistant BC cell proliferation, migration, cisplatin resistance and facilitated apoptosis. Next, we discovered that PTENP1 was a sponge of miR-103a, while PDCD4 was a target of miR-103a. More importantly, PTENP1 regulated DDP-resistant cell viability, migration, apoptosis and cisplatin resistance by interacting with the miR-103a/PDCD4 axis. In addition, PTENP1 hindered tumor growth of cisplatin-resistant mice. Exosome-derived PTENP1 suppressed the DDP resistance of BC by inhibiting cell proliferation, migration and promoting apoptosis through regulating the miR-103a/PDCD4 axis, representing a targeted therapy for DDP-resistant BC patients.
引用
收藏
页码:37642 / 37651
页数:10
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