LncRNA BLACAT1 is involved in chemoresistance of non‑small cell lung cancer cells by regulating autophagy
| Autor: | Qiang Peng, Feng‑Xiang Huang, Fu‑Xia Zheng, Ying Liu, Chang Zhao, Li‑Jun Miao, Xiang Deng, Hong‑Jie Chen, Pan‑Feng Sun, Ya‑Hui Huang, Zeng‑Yan Gao |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Cancer Research Small interfering RNA Lung Neoplasms Cell Survival Cell Biology Autophagy-Related Protein 7 03 medical and health sciences Mice 0302 clinical medicine Carcinoma Non-Small-Cell Lung Cell Line Tumor microRNA medicine Autophagy Animals Humans Viability assay Cell Proliferation A549 cell Oncogene Cell growth Cell cycle respiratory tract diseases Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology medicine.anatomical_structure Oncology A549 Cells Drug Resistance Neoplasm 030220 oncology & carcinogenesis Cancer research RNA Long Noncoding Cisplatin Neoplasm Transplantation Signal Transduction |
| Zdroj: | International journal of oncology. 54(1) |
| ISSN: | 1791-2423 |
| Popis: | The aim of the present study was to determine the effect of the long non‑coding RNA (lncRNA) bladder cancer‑associated transcript 1 (BLACAT1) in chemoresistance of non‑small cell lung cancer (NSCLC) cells. Expression of lncRNA BLACAT1, microRNA (miR)‑17, autophagy‑related protein 7 (ATG7), multidrug‑resistance protein 1 (MRP1), and the autophagy‑associated proteins light chain 3 (LC3)‑II/LC3‑I and Beclin 1 were detected using the reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Cell viability was determined using an MTT assay. The interaction between BLACAT1 and miR‑17 was determined using RNA immunoprecipitation and RNA pull‑down assays. A cisplatin (DDP)‑resistant NSCLC cell A549/DDP xenograft model in nude mice was established to investigate the effect of BLACAT1 on the chemoresistance of NSCLC cells. Compared with in DDP‑sensitive NSCLC cells, expression of BLACAT1, ATG7, MRP1, LC3‑II/LC3‑I and Beclin 1 was significantly upregulated in DDP‑resistant NSCLC cells, whereas miR‑17 was downregulated in DDP‑resistant NSCLC cells. Short interfering RNA against BLACAT1 decreased the viability of DDP‑resistant NSCLC cells. In addition, BLACAT1 interacted with miR‑17, and negatively regulated miR‑17. BLACAT1 promoted ATG7 expression through miR‑17, and facilitated autophagy and promoted chemoresistance of NSCLC cells through miR‑17/ATG7. Finally, in vivo experiments indicated that inhibition of BLACAT1 ameliorated the chemoresistance of NSCLC. BLACAT1 was upregulated in DDP‑resistant NSCLC cells, and promoted autophagy and chemoresistance of NSCLC cells through the miR‑17/ATG7 signaling pathway. |
| Databáze: | OpenAIRE |
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