Literature DB >> 25400730

γ-terpineol inhibits cell growth and induces apoptosis in human liver cancer BEL-7402 cells in vitro.

Zi-Li Wu1, Zhong-Qiong Yin2, Yong-Hua Du1, Rui-Zhang Feng1, Kui-Chuan Ye2, Qin Wei1, Yong Hu3, Lin He1, Lin Liao1, Yu Wang1.   

Abstract

To investigate the effect of γ-terpineol on cell proliferation and apoptosis of human hepatoma BEL-7402 cells to elucidate its molecular mechanism. Here, BEL-7402 cells were treated with various concentrations (40, 80, 160, 320 and 640 μg/ml) of γ-terpineol for 48 h, cell proliferation was determined by 3-(4,5-dimethyl-thiazolyl-2)-2,5-diphenyl tetrazolium bromides (MTT) assay. Cell colony inhibition was determined by soft agar assay. Apoptosis and possible molecular mechanisms were evaluated by morphological observation, flow cytometry analysis, and DNA fragmentation assay. The γ-terpineol significantly suppressed BEL-7402 cell proliferation in a dose-dependent manner. Characteristic morphological and biochemical changes associated with apoptosis such as cells shrinkage, deformation and vacuolization of mitochondria, nuclear chromatin condensation and fragmentation, formation of apoptotic bodies were observed after BEL-7402 cells treated with γ-terpineol for 24 h and 48 h. Cell cycle were displayed by flow cytometry analysis, the γ-terpineol treatment resulted in accumulation of cells at G₁ or S phase and a blockade of cell proliferation compared to control group. Treating BEL-7402 cells with 320 μg/ml of γ-terpineol for 36 h and 48 h, a typical apoptotic "DNA ladder" was observed using DNA fragmentation assay. The present study demonstrated that possible anti-cancer mechanism of γ-terpineol on human hematomas cells is through inducing cell apoptosis to suppress tumor cell growth.

Entities:  

Keywords:  BEL-7402; apoptosis; cell proliferation; human hepatoma; γ-terpineol

Mesh:

Substances:

Year:  2014        PMID: 25400730      PMCID: PMC4230123     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


  14 in total

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