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Effect of parthenolide on proliferation and apoptosis in gastric cancer cell line SGC7901
Author(s) -
ZHAO Li Jie,
XU Yong Hong,
LI Yan
Publication year - 2009
Publication title -
journal of digestive diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 51
eISSN - 1751-2980
pISSN - 1751-2972
DOI - 10.1111/j.1751-2980.2009.00382.x
Subject(s) - apoptosis , propidium iodide , annexin , cytochrome c , rhodamine 123 , microbiology and biotechnology , programmed cell death , flow cytometry , caspase , mitochondrion , cell growth , isothiocyanate , cell culture , biology , biochemistry , genetics , multiple drug resistance , antibiotics
OBJECTIVE: To investigate the effect of parthenolide (PAR) on proliferation and apoptosis in gastric cancer cell line SGC7901. METHODS: Human gastric cancer cell line SGC7901 cells were incubated with various concentration of PAR. After various periods of incubation, the proliferation of SGC7901 cells was assessed by 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide methyl thiazolyl tetrazolium (MTT) assay. Apoptosis was measured by the annexin V‐fluorescein isothiocyanate fluoresceine isothiocyanate (FITC)/propidium iodide (PI) double labeled staining method and the morphology of the cell was observed under a fluorescent microscope. Mitochondrial potential was measured by flow cytometry after Rhodamine 123 staining. The expressions of cytochrome C and the Bcl‐2 family of proteins, including Bcl‐2, Bax, Bid and tBid were measured by Western blot. Caspase 3 and 8 activities were measured by enzyme‐linked immunosorbent assay. RESULTS: Treatment with PAR induced apoptosis as confirmed by annexin V‐FITC/PI assay. PAR‐induced apoptosis was associated with intracellular events including the decline of mitochondrial potential, increased release of cytochrome C from the mitochondria, decreased expression of Bcl‐2, increased expression of Bax, Bid and tBid and activation of caspase 3 and 8. CONCLUSION: These results suggest that possibly via activation of the mitochondrial pathway, PAR causes mitochondrial damage leading to the release of cytochrome C and by regulating the expression of the Bcl‐2 family of proteins and activating caspases which leads to results in apoptotic cell death in SGC7901 cells. Our results might be helpful in formulating new therapeutic approaches using Chinese herbal medicine.