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- Title
敲减骨桥蛋白对吉非替尼耐药的非小细胞肺癌 PC9 细胞凋亡的研究.
- Authors
温晓星; 刘大海; 吴学辉; 王炳平; 房涛
- Abstract
Objective The aim of this study was to investigate the role and mechanism of osteopontin in mediating epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) resistance in NSCLC. Methods The PC9R cells with osteopontin knockdown was the treatment group, and untreated PC9R cells was the control group. Quantitative real time PCR (RT-qPCR) and Western blot (WB) were carried out to check the expression of osteopontin and apoptosis related proteins in NSCLC cells. Mitochondrial membrane potential measurement assay were performed to check the mitochondria fucntion. The cell counting kit-8 (CCK-8) and EdU incorporation assays were used to measure cell proliferation. Results The results showed that osteopontin was significantly up-regulated in gefitinib-resistant PC9R cells compared with PC9 cells (1.00±0.05 vs. 5.12±0.12, P<0.01). Knockdown of osteopontin induced mitochondria dysfunction and apoptosis related proteins were over expressed (8.34±0.96 vs. 48.56±3.34, P<0.05). Knockdown of osteopontin inhibted PC9R cells prolifereation. Therefore, our results further demonstrated osteopontin promted PC9R cells apoptosis. Conclusion Knockdown osteopontin induced mitochondrial dysfunction and induced the apoptosis of gefitinib-resistant cells. Knockdown osteopontin increases the sensitivity of lung cancer cells to gefitinib.
- Subjects
MITOCHONDRIAL physiology; LUNG cancer prevention; CYTOKINES; LUNG cancer; REVERSE transcriptase polymerase chain reaction; WESTERN immunoblotting; MITOCHONDRIAL pathology; APOPTOSIS; GENE expression; GEFITINIB; PROTEIN-tyrosine kinase inhibitors; MITOCHONDRIA; GENE expression profiling; CELL proliferation; CELL lines; DRUG resistance in cancer cells; MEMBRANE potential
- Publication
Practical Oncology Journal, 2022, Vol 36, Issue 4, p310
- ISSN
1002-3070
- Publication type
Article
- DOI
10.11904/j.issn.1002-3070.2022.04.004