Email updates

Keep up to date with the latest news and content from BMC Cell Biology and BioMed Central.

Open Access Research article

Lentivirus-mediated RNA interference targeting the H19 gene inhibits cell proliferation and apoptosis in human choriocarcinoma cell line JAR

Li-Li Yu1, Kai Chang1, Lin-Shan Lu1, Dan Zhao1, Jian Han1, Ying-Ru Zheng1, Yao-Hua Yan1, Ping Yi1, Jian-Xin Guo1, Yuan-Guo Zhou2, Ming Chen1* and Li Li1*

Author Affiliations

1 Department of Obstetrics and Gynecology, Daping Hospital, The Third Military Medical University, Chongqing 400042, China

2 Molecular Biology Center, Institute of Surgery Research, Daping Hospital, The Third Military Medical University, Chongqing 400042, China

For all author emails, please log on.

BMC Cell Biology 2013, 14:26  doi:10.1186/1471-2121-14-26

Published: 27 May 2013

Abstract

Background

H19 is a paternally imprinted gene that has been shown to be highly expressed in the trophoblast tissue. Results from previous studies have initiated a debate as to whether noncoding RNA H19 acts as a tumor suppressor or as a tumor promotor in trophoblast tissue. In the present study, we developed lentiviral vectors expressing H19-specific small interfering RNA (siRNA) to specifically block the expression of H19 in the human choriocarcinoma cell line JAR. Using this approach, we investigated the impact of the H19 gene on the proliferation, invasion and apoptosis of JAR cells. Moreover, we examined the effect of H19 knockdown on the expression of insulin-like growth factor 2 (IGF2), hairy and enhancer of split homologue-1 (HES-1) and dual-specific phosphatase 5 (DUSP5) genes.

Results

H19 knockdown inhibited apoptosis and proliferation of JAR cells, but had no significant impact on cell invasion. In addition, H19 knockdown resulted in significant upregulation of HES-1 and DUSP5 expression, but not IGF2 expression in JAR cells.

Conclusions

The finding that H19 downregulation could simultaneously inhibit proliferation and apoptosis of JAR cells highlights a putative dual function for H19 in choriocarcinoma and may explain the debate on whether H19 acts as a tumor suppressor or a tumor promotor in trophoblast tissue. Furthermore, upregulation of HES-1 and DUSP5 may mediate H19 downregulation-induced suppression of proliferation and apoptosis of JAR cells.

Keywords:
H19; JAR cells; Choriocarcinoma; HES-1; DUSP5; IGF2