Elevation of FGD5-AS1 contributes to cell progression by improving cisplatin resistance against non-small cell lung cancer cells through regulating miR-140-5p/WEE1 axis.

Non-small cell lung cancer (NSCLC) is a common lung cancer with high mortality worldwide. Cisplatin (DDP) resistance is a huge limitation for NSCLC therapy. FGD5 antisense RNA 1 (FGD5-AS1) was recognized as a significant cancer cell regulator. However, the molecular mechanism of FGD5-AS1 in cisplatin resistance of NSCLC cells is poorly understood. FGD5-AS1 and WEE1 expression were up-regulated in DDP-resistant tumors and cells compared with DDP-sensitive ones. Interestingly, down-regulation of FGD5-AS1 or WEE1 inhibited cell proliferation, migration, invasion, autophagy and stimulated cell apoptosis in NSCLC DDP-resistant cells. What's more, restoration of WEE1 abrogated FGD5-AS1 silencing-induced suppression on cell proliferation, migration, invasion, autophagy and promotion on cell apoptosis in NSCLC DDP-resistant cells. Next, we discovered that FGD5-AS1 was able to enhance WEE1 expression by interacting with miR-140-5p. Furthermore, FGD5-AS1 silencing restrained tumor growth of cisplatin-resistant mice. Overexpression of FGD5-AS1 accelerated cell proliferation, migration, invasion and autophagy by enhancing cisplatin resistance against NSCLC cells through miR-140-5p/WEE1 axis, presenting promising biomarkers for the diagnosis of DDP-resistant NSCLC patients.

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