LINC00511 Knockdown Suppresses Resistance to Cisplatin in Lung Adenocarcinoma by Interacting with miR-182-3p and BIRC5
Autor: | Zhongcheng Zhu, Mingyun Zhang, Yufeng Shi, Xiaoyi Gong, Jing Li |
---|---|
Rok vydání: | 2021 |
Předmět: |
Male
endocrine system diseases Survivin Down-Regulation Bioengineering Adenocarcinoma of Lung Inhibitor of apoptosis medicine.disease_cause Applied Microbiology and Biotechnology Biochemistry Mice In vivo Cell Line Tumor medicine Animals Humans Viability assay RNA Small Interfering Molecular Biology A549 cell Cisplatin Gene knockdown Chemistry respiratory system Xenograft Model Antitumor Assays respiratory tract diseases Up-Regulation Gene Expression Regulation Neoplastic MicroRNAs Apoptosis A549 Cells Drug Resistance Neoplasm Cancer research Female RNA Long Noncoding Carcinogenesis Biotechnology medicine.drug |
Zdroj: | Molecular biotechnology. 64(3) |
ISSN: | 1559-0305 |
Popis: | We studied the role of long intergenic non-protein coding RNA 00,511 (LINC00511) in lung adenocarcinoma (LUAD), with a specific focus on acquired chemoresistance. LINC00511 expression was higher in responders to cisplatin (DDP, another name for cisplantin) than non-responders, in A549/DDP cells than in parental A549 cells and normal human bronchial epithelial cells (16HBE). LINC00511 knockdown decreased the half maximal inhibitory concentration (IC50) value, suppressed A549/DDP cell viability, but induced apoptosis. LINC00511 bound with miR-182 and increased the expression of baculoviral inhibitor of apoptosis protein (IAP) repeat containing 5 (BIRC5). BIRC5 knockdown mimicked the effects of LINC00511 knockdown on the IC50 value, A549/DDP cell viability, and apoptosis. BIRC5 overexpression negated the effects of LINC00511 knockdown on A549/DDP cells. In vivo, LINC00511 knockdown attenuated the tumorigenesis of A549/DDP cells after DDP injection. These results provide a novel LINC00511/miR-182/BIRC5 paradigm to explain the mechanism of acquired DDP resistance. |
Databáze: | OpenAIRE |
Externí odkaz: |