Abstract
Sex hormones from environmental and physiological sources might play a major role in the pathogenesis of hepatoblastoma in children. This study investigated the effects of estradiol and bisphenol A on the proliferation and telomerase activity of human hepatoblastoma HepG2 cells. The cells were divided into 6 treatment groups: control, bisphenol A, estradiol, anti-estrogen ICI 182,780 (hereinafter ICI), bisphenol A+ICI, and estradiol+ICI. Cell proliferation was measured based on average absorbance using the Cell Counting-8 assay. The cell cycle distribution and apoptotic index were determined by flow cytometry. Telomerase activity was detected by polymerase chain reaction and a telomeric repeat amplification protocol assay. A higher cell density was observed in bisphenol A (P<0.01) and estradiol (P<0.05) groups compared with the control group. Cell numbers in S and G2/M phases after treatment for 48 h were higher (P<0.05), while the apoptotic index was lower (P<0.05) and telomerase activities at 48 and 72 h (P<0.05) were higher in these groups than in the control group. The cell density was also higher in bisphenol A+ICI (P<0.01) and estradiol+ICI (P<0.05) groups compared with the ICI group. Furthermore, cell numbers were increased in S and G2/M phases (P<0.05), while the apoptotic index was lower (P<0.05) and telomerase activities at 48 and 72 h were higher (P<0.05) in these groups than in the ICI group. Therefore, bisphenol A and estradiol promote HepG2 cell proliferation in vitro by inhibition of apoptosis and stimulation of telomerase activity via an estrogen receptor-dependent pathway.
Highlights
Hepatoblastoma (HB) is the most common malignant, solid liver tumor in children, arising from multipotent stem cells that differentiate into liver and bile duct epithelial cells in undifferentiated embryonic tissue [1]
This study investigated the effects of estradiol and bisphenol A on the proliferation and telomerase activity of human hepatoblastoma HepG2 cells
This study investigated the effects of physiological and environmental estrogen on HB by treating human hepatoblastoma HepG2 cells with 17b-estradiol (E2) and bisphenol A (BPA), and evaluating cell proliferation, apoptosis, and telomerase activity
Summary
Hepatoblastoma (HB) is the most common malignant, solid liver tumor in children, arising from multipotent stem cells that differentiate into liver and bile duct epithelial cells in undifferentiated embryonic tissue [1]. It accounts for about 25% of pediatric liver tumors and 50–69% of malignant hepatic tumors among primary embryonal tumors [2]. Estrogen maintains the function of sex organs and regulates metabolism in humans [5]. Another study has suggested that estrogen promotes angiogenesis and, the proliferation of hemangiomas in children [12]. There is little known about the role of estrogen in hepatoblastoma
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