Tumor suppressor miR‑613 induces cisplatin sensitivity in non‑small cell lung cancer cells by targeting GJA1
- Jianhua Luo
- Yan Jin
- Mengyuan Li
- Liyang Dong
Affiliations: Department of Respiratory Medicine, Taizhou Municipal Hospital, Taizhou, Zhejiang 318000, P.R. China, Department of Invasive Technology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China
- Published online on: March 18, 2021 https://doi.org/10.3892/mmr.2021.12024
Copyright: © Luo
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:
It has been reported that microRNAs (miRs) contribute to several biological functions and are associated with drug resistance in various types of cancer. However, to the best of our knowledge, whether miR‑613 can affect cisplatin (CDDP) sensitivity in non‑small cell lung cancer (NSCLC) remains unknown. Reverse transcription‑quantitative PCR was performed to detect the expression levels of miR‑613 and gap junction α‑1 protein (GJA1) in patients with NSCLC. Cell Counting Kit‑8, colony formation and Transwell assays were employed to exam the effects of miR‑613 and GJA1 on cell functions. Cell apoptosis was analyzed using flow cytometry. An in vivo experiment was conducted to determine the influence of miR‑613 on tumor formation. In the present study, miR‑613 was revealed to be significantly downregulated in lung cancer tissues compared with in adjacent normal tissues, and low miR‑613 expression indicated a poor prognosis. Furthermore, cell proliferation, colony formation and migration of lung cancer cells were inhibited by overexpression of miR‑613. In vivo experiments also demonstrated that miR‑613 could inhibit tumor growth. Moreover, miR‑613 could enhance the negative effects of CDDP on cell proliferation, apoptosis and migration. GJA1 was revealed to be a target gene of miR‑613 and was upregulated in human lung cancer tissues. Rescue experiments demonstrated that miR‑613 increased the chemosensitivity of lung cancer cells by targeting GJA1. Collectively, the results suggested a tumor suppressor role of miR‑613 in NSCLC and indicated that miR‑613 could strengthen CDDP sensitivity in NSCLC cells by targeting GJA1, which may provide a novel therapeutic target for NSCLC.