期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 504, 期 1, 页码 123-128出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2018.08.142
关键词
Paclitaxel; NSCLC; A549; MEG3; P53
资金
- Bureau of Public Health of Jiangsu Province [H201413]
- preresearch project from the Second Affiliated Hospital of Soochow University [SDFEYGJ1609]
- Second Affiliated Hospital of Soochow University clinical discipline group project funding [XKQ 2015008]
- National Science Foundation of Jiangsu Province [BK20150302]
- Clinical Pharmacy Foundation of Jiangsu Pharmaceutical Association [201509]
- Health Bureau of Suzhou [SYZ201632, SS201641]
- Program for Diagnostic and Therapeutic Technique of Clinical Important Disease in Suzhou [LCZX201707]
Paclitaxel (PTX) is a first-line chemotherapy drug for advanced non-small cell lung cancer (NSCLC). The long-chain non-coding RNA maternally expressed gene 3 (MEG3) is a recognized tumor suppressor. This study aimed to explore the effects of PTX on the expression of MEG3 and its anti-tumor mechanism in lung cancer cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were performed to determine cell proliferation. Quantitative polymerase chain reaction was used to determine the levels of MEG3 expressions. Western blot and immunofluorescence were used to detect protein levels. Small interfering RNA or pCDNA-MEG3 transfection was used to downregulate or upregulate MEG3 expression. Dichlorof luorescein diacetate was used to detect intracellular reactive oxygen species. Flow cytometry was used to analyze apoptosis. PTX significantly inhibited the proliferation of NSCLC cells and increased the expressions of MEG3 and P53. The downregulation of MEG3 attenuated PTX-induced cytotoxicity, whereas upregulation of MEG3 induced cell death and increased P53 expression. The inhibition of P53 caused no effect on the upstream MEG3 expression. Our results suggest that the MEG3-P53 pathway is involved in the apoptosis of A549 cells induced by PTX. (C) 2018 Elsevier Inc. All rights reserved.
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