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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Downregulation of Linc00173 increases BCL2 mRNA stability via the miR-1275/PROCA1/ZFP36L2 axis and induces acquired cisplatin resistance of lung adenocarcinoma

Fig. 6

LINC00173 mediated chemosensitivity to DDP in LUAD via PROCA1/ZFP36L2/BCL2 axis. a. The protein level of PROCA1, BCL-2, PARP, cleaved-PARP (c-PARP), Caspase3 and cleaved-Caspase3 (c-CASP3) in LINC00173 transfected A549-DDP and PC9-DDP cells (cultured with cisplatin) were examined by western blot. GAPDH and β-Tubulin were used as loading controls. b. Co-immunoprecipitation analysed the level of PROCA1 binding to ZFP36L2 in A549 and A549-DDP cells (cultured with cisplatin) transfected with shLINC00173 or LINC00173, respectively. c and d. BCL2 mRNA degradation was monitored by qRT-PCR in A549-shLINC00173 (c) or A549-DDP-LINC00173 cells cultured with cisplatin (d). e. The expression of LINC00173 in xenograft tumor tissues generated from A549 cells expressing either shRNAs targeting LINC00173 (shLINC00173-1) or nontargeting shRNA (scramble) and treated with cisplatin or control normal saline (N.S) f. The protein levels of PROCA1, ZFP36L2, and BCL2 in xenograft tumor tissues generated from A549 cells expressing either shRNAs targeting LINC00173 (shLINC00173-1) or nontargeting shRNA (scramble) and treated with cisplatin or control normal saline (N.S). Student’s two-tailed t-test, *P < 0.05; **P < 0.01; ***P < 0.001. Error bars, mean ± SD

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