Open Access

ARTICLE

Overexpression of inhibin α (1-32) fusion protein promotes apoptosis and cell cycle arrest in a cervical cancer cell model (Hela cells)

Yanhong ZHEN¹, Li HAN², Kailai CAI¹, Lijun HUO¹, Hasan RIAZ¹, Canjie WU¹, Aixin LIANG¹ , Lei SANG¹, Liguo YANG^{1 *}

1 Key laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education. Huazhong Agricultural University, Wuhan, 430070, Hubei, China.
2 College of Animal Science and Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei 430070, China

* Address correspondence to: Liguo Yang,

BIOCELL 2014, 38(1), 17-24. https://doi.org/10.32604/biocell.2014.38.017

Abstract

Inhibins play important roles in the reproductive system. To evaluate whether inhibin α (1-32) fusion protein plays a role in cervical cancer growth, the plasmid pVAX-inhα was constructed and its effect on proliferation and apoptosis of the human cervical cancer cell line (Hela) was checked by flow cytometry and real-time PCR. The expression and localization of inhibin α protein were detected by RT-PCR and confocal microscopy which showed that inhibin α protein was expressed and localized in the nucleus of Hela cells. Over expression of inhibin α gene significantly induced cell apoptosis and ceased S phase of cell cycle. Furthermore, cell proliferation was significantly suppressed 96 h post-transfection and mRNA level of anti-apoptosis genes (Bcl-2, NFκB) were decreased but pro-apoptosis genes (Bax, wild type p53) and inhibin co receptor (TGFβR3) were increased, indicating that inhibin, through its co-receptor, might activate apoptotic and cell growth cascades which regulate proliferation and apoptosis in Hela cells. These results suggest that inhibin α (1-32) fusion protein, located in the cell nucleus, can regulate Hela cells growth and apoptosis by induction of apoptotic pathways such as NFκB, Bcl-2 and p53 families. These findings may have a significant impact on future research regarding cervical cancer cell lines

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