1. Long non-coding RNA prostate cancer-associated transcript 6 inhibited gefitinib sensitivity of non-small cell lung cancer by serving as a competing endogenous RNA of miR-326 to up-regulate interferon-alpha receptor 2.
- Author
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Zheng Y, Guo Z, and Li Y
- Subjects
- Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung genetics, Cell Line, Tumor, Humans, Lung Neoplasms drug therapy, Lung Neoplasms genetics, MicroRNAs genetics, Neoplasm Proteins genetics, RNA, Long Noncoding genetics, RNA, Neoplasm genetics, Receptor, Interferon alpha-beta genetics, Carcinoma, Non-Small-Cell Lung metabolism, Gefitinib pharmacology, Gene Expression Regulation, Neoplastic drug effects, Lung Neoplasms metabolism, MicroRNAs biosynthesis, Neoplasm Proteins biosynthesis, RNA, Long Noncoding biosynthesis, RNA, Neoplasm biosynthesis, Receptor, Interferon alpha-beta biosynthesis, Up-Regulation drug effects
- Abstract
The critical roles of lncRNAs in drug resistance of malignancies have been widely recognized. This investigation aims to study the function of lncRNA PCAT6 in the resistance of non-small cell lung cancer (NSCLC) to gefitinib. In our study, we demonstrated that prostate cancer-associated transcript 6 (PCAT6) was upregulated in gefitinib-resistant NSCLC. PCAT6 knockdown inhibited gefitinib resistance of NSCLC, as indicated by decreased IC
50 value, proliferation, and metastasis, and increased cell apoptosis. Besides, PCAT6 could directly target miR-326 in gefitinib-resistant NSCLC cells and augment NSCLC resistance to gefitinib by serving as ceRNA of miR-326. Furthermore, interferon-alpha receptor 2 (IFNAR2) was validated as a downstream target of miR-326 and miR-326 reduced resistance to gefitinib by inhibiting IFNAR2 expression. Our investigation identified that PCAT6 enhanced gefitinib resistance of NSCLC via miR-326/IFNAR2 axis, which might offer a new therapeutic strategy against gefitinib resistance of NSCLC patients.- Published
- 2022
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