Fig. 4

Knock-down of circRNA CDR1as sensitized DDP-resistant NSCLC cells to by regulating miR-641/HOXA9 axis. The a circRNA CDR1as downregulation vectors, b miR-641 inhibitor and c HOXA9 overexpression vectors were successfully delivered into DDP-resistant NSCLC cells, examined by Real-Time qPCR. d CCK-8 assay and e trypan blue assay results indicated that circRNA CDR1as deficiency aggravated the inhibiting effects of DDP on DDP-resistant NSCLC cell proliferation and viability by downregulating HOXA9 through upregulating miR-641. f Annexin V-FITC/PI double stain method combined with flow cytometer (FCM) revealed that knock-down of circRNA CDR1as increased apoptosis ratio in DDP treated A549/DDP, H1299/DDP and Calu6/DDP cells by regulating miR-641/HOXA9 axis. g The xenograft tumor bearing mice models were established to evaluate the tumorigenicity of NSCLC cells in vivo. (Note: “D” represented “DDP”, “KD-C” represented “circRNA CDR1as silence”, “KD-miR” represented “miR-641 ablation” and “OE-H” meant “overexpression of HOXA9”). Each experiment repeated at least 3 times. *P < 0.05, **P < 0.01. “NS” represented no statistical significance