miR-365a-5p suppresses gefitinib resistance in non-small-cell lung cancer through targeting PELI3

Author:

Li Fannian1,Li Haitao2,Li Shuai2,Lv Baolei3,Shi Junjie4,Yan Hongjiang5,Zhang Helin5,He Yuzheng5

Affiliation:

1. Department of Thoracic Surgery, The First Hospital of XingTai, No. 376 Shunde Road, XingTai, Hebei, 054001, China

2. Department of Pulmonary & Critical Care Medicine, The Second Hospital of Hebei Medical University, No. 215 Heping West Road, Shijiazhuang, Hebei, 050000, China

3. Department of Thoracic Surgery, The First Hospital of Shijiazhuang, No. 36 Fanxi Road, Chang’an District, Shijiazhuang, Hebei, 050011, China

4. Department of Thoracic Surgery, Handan First Hospital, No. 25 CongTai Road, HanDan, 056002, China

5. Department of Thoracic Surgery, The Second Hospital of Hebei Medical University, No. 215 Heping West Road, Shijiazhuang, Hebei, 050000, China

Abstract

Aim: Demonstrate the function of dysregulated miR-365a-5p–PELI3 signaling axis in the generation of gefitinib resistance during treatment for non-small-cell lung cancer (NSCLC). Patients & methods: All the NSCLC patients who participated in this research were recruited from the Second Hospital of Hebei Medical University. PC9 cells and PC9GR cells were cultured for in vitro experiments. Results: Patients who were primary resistant to EGFR-tyrosine kinase inhibitor had lower miR-365a-5p levels. MiR-365a-5p directly targeted PELI3 mRNA. MiR-365a-5p overexpression enhanced the function of gefitinib in inhibiting cell viability. Tumor growth was suppressed through miR-365a-5p in nude mice. Conclusion: Dysregulated miR-365a-5p–PELI3 signaling axis triggered the generation of gefitinib resistance in NSCLC.

Publisher

Future Medicine Ltd

Subject

Pharmacology,Genetics,Molecular Medicine

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