FGD5‑AS1 promotes cisplatin resistance of human lung adenocarcinoma cell via the miR‑142‑5p/PD‑L1 axis
- Feng Zhu
- Rong Niu
- Xiaoliang Shao
- Xiaonan Shao
Affiliations: Department of Respiratory and Critical Care Medicine, Wuxi Fifth People's Hospital, Wuxi, Jiangsu 214000, P.R. China, Department of Nuclear Medicine, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213003, P.R. China
- Published online on: December 14, 2020 https://doi.org/10.3892/ijmm.2020.4816
Copyright: © Zhu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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.