Anticancer roles of let-7f-1-3p in non-small cell lung cancer via direct targeting of integrin β1

Yanan Yang; Yuanrong Liu; Ning Xie; Liying Shao; Hang Sun; Yubo Wei; Yunxiao Sun; Pingyu Wang; Yunfei Yan; Shuyang Xie; Youjie Li

doi:10.3892/etm.2021.10740

Anticancer roles of let-7f-1-3p in non-small cell lung cancer via direct targeting of integrin β1

Exp Ther Med. 2021 Nov;22(5):1305. doi: 10.3892/etm.2021.10740. Epub 2021 Sep 16.

Authors

Yanan Yang¹, Yuanrong Liu¹, Ning Xie², Liying Shao¹, Hang Sun¹, Yubo Wei¹, Yunxiao Sun³, Pingyu Wang¹, Yunfei Yan¹, Shuyang Xie¹, Youjie Li¹

Affiliations

¹ Key Laboratory of Tumor Molecular Biology, Department of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, Shandong 264003, P.R. China.
² Department of Thoracic Surgery, Yantaishan Hospital, Yantai, Shandong 264001, P.R. China.
³ Department of Pediatrics, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong 264100, P.R. China.

Abstract

Lung cancer is one of the most common types of cancer, with the highest mortality rate worldwide. MicroRNAs play notable roles in the chemotherapeutic effects of anticancer drugs. The present study used reverse transcription-quantitative PCR, western blotting and cell migration and invasion assays to reveal the role of let-7f-1-3p in non-small cell lung cancer (NSCLC) and explore the effect of let-7f-1-3p on doxorubicin (DOX) treatment. It was demonstrated that the levels of let-7f-1-3p in carcinoma tissues were lower compared with those in paracarcinoma tissues. Thus, let-7f-1-3p may act as a suppressor gene. The present study also explored the role of let-7f-1-3p in A549 and NCI-H1975 cells. Results revealed that let-7f-1-3p could inhibit the viability, migration and invasion of NSCLC cells and induce their apoptosis. Integrin β1 acted as a target gene regulated by let-7f-1-3p. This suggested that let-7f-1-3p could enhance DOX-inhibited cell viability, migration and invasion in vitro. Overall, the present study demonstrated that let-7f-1-3p may act as a target for drug design and lung cancer therapy.

Keywords: DOX; ITGB1; NSCLC; chemotherapy; let-7f-1-3p.

Grants and funding

Funding: The present study was supported by National Natural Science Foundation of China (grant nos. 81800169, 81772281 and 81702296), Shandong Science and Technology Committee (grant nos. 2018GSF118056 and ZR2019MH022), Foundation of Shandong Educational Committee (grant nos. J17KA121 and 2019KJK014), Yantai Science and Technology Committee (grant no. 2018XSCC051) and Shandong Province Taishan Scholar Project (grant no. ts201712067).