MicroRNA-130a-3p regulates osimertinib resistance by targeting runt-related transcription factor 3 in lung adenocarcinoma

Author:

Shintani Takuya1,Shun Yu-Ting2,Toyozumi Yuji2,Ikemura Kenji1,Takeda Yoshito2,Shiroyama Takayuki2,Nagatomo Izumi2,Kumanogoh Atsushi2,Okuda Masahiro1,Jingushi kentaro2

Affiliation:

1. Osaka University Hospital

2. Osaka University

Abstract

Abstract

Overcoming resistance to epidermal growth factor receptor tyrosine kinase inhibitors, including osimertinib, is urgent to improve lung cancer treatment outcomes. Extracellular vesicle (EV)-derived microRNAs (EV-miRNAs) play important roles in drug resistance and serve as promising biomarkers. In this study, we aimed to identify EV-miRNAs associated with osimertinib resistance and investigate their clinical relevance. The release of excess EVs was confirmed in an osimertinib-resistant lung adenocarcinoma cell line (PC9OR). The exposure of EVs and EV-miRNAs derived from PC9OR cells to PC9 cells increased cell viability after osimertinib treatment. Microarray analysis revealed that miR-130a-3p was upregulated in EVs derived from PC9OR cells and another osimertinib-resistant cell line (H1975OR). Transfection with miR-130a-3p attenuated osimertinib-induced cytotoxicity and apoptosis in both PC9 and H1975 cells, whereas osimertinib resistance in PC9OR cells was reversed after miR-130a-3p inhibition. Bioinformatics analysis revealed that runt-related transcription factor 3 is a target gene of miR-130a-3p, and it induced osimertinib resistance in PC9 cells. Finally, patients with lower baseline serum miR-130a-3p concentrations had longer progression-free survival. miR-130a-3p is a potential therapeutic target and a predictive biomarker of osimertinib resistance in adenocarcinoma.

Publisher

Springer Science and Business Media LLC

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