FGD5-AS1 promotes cisplatin resistance of human lung adenocarcinoma cell via the miR-142-5p/PD-L1 axis

Previous studies have reported that long non-coding (lnc) RNA FGD5-antisense 1 (FGD5-AS1) promotes tumor proliferation, migration and invasion. Therefore, the present study aimed to elucidate the biological role and underlying molecular mechanisms of FGD5-AS1 in cisplatin (DDP) resistance of lung adenocarcinoma (LAD) cells. The results demonstrated that FGD5-AS1 was highly expressed in DDP-resistant LAD tissues and cells. Knockdown of FGD5-AS1 decreased the proliferative, migratory and invasive abilities of DDP-resistant LAD cells. Moreover, it was identified that FGD5-AS1 acted as a molecular sponge for microRNA (miR)-142, and FGD5-AS1 enhanced the resistance of A549/DDP cells to DDP by directly interacting with miR-142. Programmed cell death 1 ligand 1 (PD-L1) was also found to be a key effector of the FGD5-AS1/miR-142 axis to regulate the chemoresistance of DDP-resistant LAD cells. In conclusion, the present study demonstrated that FGD5-AS1 increased DDP resistance of LAD via the miR-142/PD-L1 axis, which may offer a novel treatment strategy for patients with DDP-resistant LAD.

Automated summary

The study revealed that FGD5-AS1 increases resistance of LAD to DDP via the miR-142/PD-L1 axis, suggesting a novel treatment approach for patients with DDP-resistant LAD.