NDLI: Gallic acid induces apoptosis and enhances the anticancer effects of cisplatin in human small cell lung cancer H446 cell line via the ROS-dependent mitochondrial apoptotic pathway.

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Gallic acid induces apoptosis and enhances the anticancer effects of cisplatin in human small cell lung cancer H446 cell line via the ROS-dependent mitochondrial apoptotic pathway.

Content Provider	Semantic Scholar
Author	Wang, Ruixuan Ma, Lijie Weng, Dan Yao, Jiahui Liu, Xueying Jin, Faguang
Copyright Year	2016
Abstract	Small cell lung cancer (SCLC) is the most aggressive lung cancer subtype and accounts for more than 15% of all lung cancer cases. Cisplatin [cis-diamminedichloroplatinum (CDDP)]-based combination chemotherapy is the cornerstone for all stages of SCLC. However, acquired multidrug resistance (MDR) and intolerable toxicities lead to a high mortality rate in SCLC patients. Gallic acid [3,4,5-trihydroxybenzoic acid (GA)] is a natural botanic phenolic compound which can induce cell apoptosis in several types of cancers. In the present study, we aimed to explore the anticancer effects of GA on human SCLC H446 cells and its promotive effects on the anticancer activities of cisplatin. The viability of the H446 cells was analyzed by MTT assay. Morphological changes in the H446 cells were observed under an inverted microscope. Apoptosis induction was determined by Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining. The level of reactive oxygen species (ROS) was assessed by 2'7'-dichlorofluorescein diacetate (DCFH‑DA), mitochondrial membrane potential (MMP) by JC-1, and western blotting was used to examine the expression of mitochondrial apoptosis-related proteins. The results showed that both GA and cisplatin changed the morphology, inhibited the growth and induced apoptosis in the H446 cells by inducing generation of ROS, disruption of MMP, downregulation of XIAP expression, and upregulation of Bax, Apaf-1, DIABLO and p53 expression. More importantly, GA combined with cisplatin exhibited synergistic effects on inducing of these pro-apoptotic mediators and modulating the activation of apoptosis-related molecules. However, inhibition of the generation of ROS by N-acetyl-l-cysteine (NAC), a specific ROS inhibitor, reversed the cell apoptosis induced by cisplatin combined with GA. In conclusion, the results from the present study revealed that GA exhibited an anticancer effect on human SCLC H446 cells and enhanced the antitumor activities of cisplatin via the ROS-dependent mitochondrial apoptotic pathway.
Starting Page	895
Ending Page	902
Page Count	8
File Format	PDF HTM / HTML
Alternate Webpage(s)	https://www.spandidos-publications.com/or/35/5/3075/download
PubMed reference number	26987028v1
Alternate Webpage(s)	https://doi.org/10.3892/or.2016.4690
DOI	10.3892/or.2016.4690
Journal	Oncology reports
Volume Number	35
Issue Number	5
Language	English
Access Restriction	Open
Subject Keyword	APAF1 gene Acetylcysteine Adverse reaction to drug Cisplatin Cysteine DIABLO gene Down-Regulation Echothiophate Iodide Fluorescein Gallic acid Gallium Iodides Isothiocyanates Malignant Neoplasms Membrane Potential, Mitochondrial Membrane Potentials Microscope Device Component Mitochondrial Inheritance Mitochondrial Membranes Multi-Drug Resistance Non-Small Cell Lung Carcinoma Patients Positive Regulation of Apoptosis Reactive Oxygen Species Small cell carcinoma of lung Staining method Up-Regulation (Physiology) Western Blotting XIAP gene annexin A5 monooxyethylene trimethylolpropane tristearate phenethyl isothiocyanate
Content Type	Text
Resource Type	Article

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