MiR-194-5p enhances the sensitivity of nonsmall-cell lung cancer to doxorubicin through targeted inhibition of hypoxia-inducible factor-1
| Autor: | Hucheng Chen, Mengning Xia, Lili Sheng, Weigang Chen, Xue Xue, Zheng Guoyan, Wei Qu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Lung Neoplasms
RD1-811 medicine.medical_treatment Cell NSCLC Western blot Surgical oncology Cell Line Tumor medicine Humans Doxorubicin resistance Doxorubicin RC254-282 Chemotherapy TUNEL assay medicine.diagnostic_test business.industry Research HIF-1 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Hypoxia-Inducible Factor 1 alpha Subunit Prognosis Reverse transcriptase respiratory tract diseases MicroRNAs medicine.anatomical_structure Oncology Apoptosis A549 Cells Cancer research miR-194-5p Surgery Hypoxia-Inducible Factor 1 business medicine.drug |
| Zdroj: | World Journal of Surgical Oncology, Vol 19, Iss 1, Pp 1-8 (2021) World Journal of Surgical Oncology |
| ISSN: | 1477-7819 |
| Popis: | BackgroundDespite chemotherapy being a common treatment, an increase in chemoresistance over time is unavoidable. We therefore investigated the role of miR-194-5p in regulating chordoma cell behavior and examined the downstream effectors of miR-194-5p.MethodsIn this study, NSCLC cell lines A549 and H460 were cultured under hypoxic conditions for 1 week to induce drug resistance to doxorubicin (DOX). The connection between miR-194-5p and HIF-1 was revealed by reverse transcription and real-time polymerase chain reaction (RT-qPCR), western blot, and dual-luciferase assays. We used TUNEL staining and the CCK-8 test to assess the sensitivity of NSCLC cells to DOX.ResultsWe found that hypoxia-induced NSCLC cells enhanced resistance to DOX. MiR-194-5p was substantially reduced, and HIF-1 was increased in hypoxia-induced drug-resistant NSCLC cells. Moreover, miR-194-5p successfully induced NSCLC cell apoptosis by directly inhibiting HIF-1, thereby enhancing DOX sensitivity.ConclusionsMiR-194-5p enhanced the sensitivity of NSCLC cells to DOX by directly inhibiting HIF-1. This work provides insights into underlying treatments for drug-resistant NSCLC. |
| Databáze: | OpenAIRE |
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