Li Fannian, Li Haitao, Li Shuai, Lv Baolei, Shi Junjie, Yan Hongjiang, Zhang Helin, He Yuzheng
Department of Thoracic Surgery, The First Hospital of XingTai, No. 376 Shunde Road, XingTai, Hebei, 054001, China.
Department of Pulmonary & Critical Care Medicine, The Second Hospital of Hebei Medical University, No. 215 Heping West Road, Shijiazhuang, Hebei, 050000, China.
Pharmacogenomics. 2020 Jul;21(11):771-783. doi: 10.2217/pgs-2020-0006. Epub 2020 Jul 8.
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). 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 experiments. 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. Dysregulated miR-365a-5p-PELI3 signaling axis triggered the generation of gefitinib resistance in NSCLC.
证明失调的miR-365a-5p-PELI3信号轴在非小细胞肺癌（NSCLC）治疗期间吉非替尼耐药产生中的作用。所有参与本研究的NSCLC患者均来自河北医科大学第二医院。培养PC9细胞和PC9GR细胞用于实验。对EGFR-酪氨酸激酶抑制剂原发性耐药的患者miR-365a-5p水平较低。miR-365a-5p直接靶向PELI3 mRNA。miR-365a-5p过表达增强了吉非替尼抑制细胞活力的功能。在裸鼠中，通过miR-365a-5p抑制肿瘤生长。失调的miR-365a-5p-PELI3信号轴引发了NSCLC中吉非替尼耐药的产生。
