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Up-regulation of microRNA miR-101-3p enhances sensitivity to cisplatin via regulation of small interfering RNA (siRNA) Anti-human AGT4D and autophagy in non-small-cell lung carcinoma (NSCLC).

PMID: 34694211 (view PubMed database entry)
DOI: 10.1080/21655979.2021.1982274 (read at publisher's website )
PMCID: PMC8806688 (free full text version available)

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Dong Cui, Yu Feng, Rulin Qian,

The emergence of drug resistance hinders the treatment of malignant tumors, and autophagy plays an important role in tumor chemotherapy resistance. However, its mechanism in non-small cell lung cancer (NSCLC) has not been well-researched. We aim to investigate the role of miR-101-3p in cisplatin-resistant via regulation of autophagy-related protein 4D (ATG4D) and autophagy. Cell viability, apoptosis, fluorescence intensity of GFP-LC3 and RFP-GFP-LC3 were determined using Cell Counting Kit-8 (CCK-8) assay, flow cytometry, and Laser scanning confocal microscope analysis, respectively. The levels of LC3II/LC3I, P62 and ATG4D were detected by Western blot. The results showed that the sensitivity to cisplatin in NSCLC cells was up-regulated by miR-101-3p mimics treatment, inducing promoting cell apoptosis and inhibiting autophagy. Further mechanistic study identified that ATG4D was a direct target of miR-101-3p. Moreover, ATG4D siRNA also could reverse miR-101-3p inhibitor-induced the up-regulation of ATG4D and the ration of LC3II/LC3I, the down-regulation of p62 expression. Our findings indicated that miR-101-3p could regulate sensitivity to cisplatin of NSNCC cells by regulating autophagy mediated by ATG4D. Therefore, miR-101-3p may act as a potential therapeutic target for the treatment of NSCLC.

Bioengineered (Bioengineered)
[2021, 12(1):8435-8446]

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