miR-148a promotes cell sensitivity through downregulating SOS2 in radiation-resistant non-small cell lung cancer cells

5Citations
Citations of this article
13Readers
Mendeley users who have this article in their library.

Abstract

Non-small cell lung carcinoma (NSCLC) is the most common type of lung cancer; however, radioresistance is a significant barrier in NSCLC radiotherapy. MicroRNA (miR)-148a has been reported to be a tumor suppressor in various types of cancer, including NSCLC. In the present study, the potential role of miR-148a in regulating radiosen- sitivity of NSCLC cells was investigated. Serum miR-148a expression was evaluated by reverse transcription-quantitative PCR in patients with NSCLC and healthy controls. The effects of miR-148a on cell viability, migration and invasion were assessed by Cell Counting Kit-8 and Transwell assays in radiation-resistant NSCLC cells. Serum miR-148a was down- regulated in patients with NSCLC compared with healthy controls and its expression was significantly increased after radiotherapy. By contrast, miR-148a expression was decreased in the radioresistant patients compared with the radiosensitivity patients. Additionally, miR-148a overexpression inhibited the cell proliferation, migration and invasion of radiation-resistant NSCLC cells. In addition, miR-148a had putative binding site with Son of Sevenless 2 (SOS2) and negatively regulated SOS2 expression. Silencing SOS2 expression significantly suppressed miR-148a inhibitor-induced increase in radiosensi- tivity in NSCLC. In conclusion, the results of the present study suggested that miR-148a could enhance the radiosensitivity of NSCLC cells through targeting SOS2, thus providing potential therapeutic targets to improve radiotherapy in NSCLC.

Cite

CITATION STYLE

APA

Zhang, Y., & Hu, X. (2022). miR-148a promotes cell sensitivity through downregulating SOS2 in radiation-resistant non-small cell lung cancer cells. Oncology Letters, 23(4). https://doi.org/10.3892/ol.2022.13255

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free