Oncostatin M stimulates cell migration and proliferation by down-regulating E-cadherin in HTR8/SVneo cell line through S
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RESEARCH
Open Access
Oncostatin M stimulates cell migration and proliferation by down-regulating E-cadherin in HTR8/SVneo cell line through STAT3 activation Hyun Sun Ko1†, Sae Kyung Choi1†, Hee Kyung Kang1, Ho Shik Kim2, Ji Hyun Jeon3, In Yang Park1 and Jong Chul Shin1*
Abstract Background: During the first trimester of pregnancy, trophoblastic E-cadherin expression is down-regulated, thereby allowing extravillous trophoblasts (EVTs) to acquire the potential for migration and invasiveness. The aim of the present study was to investigate the role of OSM on the migration and proliferation of EVT cell line HTR8/SVneo with regard to its effects on the expression of E-cadherin and STAT3 activation. Methods: We investigated the effects of OSM on RNA and protein expression of E-cadherin by real time RT-PCR analyses, western blotting, and indirect immunofluorescence staining in HTR8/SVneo cells, as well as the effects on cell migration and proliferation. The selective signal transducer and activator of transcription (STAT)3 inhibitor, stattic, and STAT3 siRNA were used to investigate STAT3 activation by OSM. Results: OSM significantly reduced RNA and protein expression of E-cadherin. Indirect immunofluorescence staining of HTR8/SVneo cells also revealed the down-regulation of E-cadherin, compared with the controls. OSM-stimulated cell migration was attenuated by anti-gp130 antibodies. OSM-induced STAT3 phosphorylation, and the down-regulation of E-cadherin by OSM treatment was restored by stattic and STAT3 siRNA. In addition, OSM-stimulated migration and proliferation were significantly suppressed by STAT3 inhibition. Conclusions: This study suggests that OSM stimulates the migration and proliferation of EVTs during the first trimester of pregnancy through the down-regulation of E-cadherin. In addition, this study suggests that the effects of OSM on migration and proliferation are related to STAT3 activation, which is important in trophoblast invasiveness. Keywords: Oncostatin M (OSM), Trophoblast, Migration, Proliferation, E-cadherin, Signal transducer and activator of transcription (STAT)3
Background In early pregnancy, extravillous trophoblasts (EVTs) invade through the endometrium, interact with decidual and immunocompetent cells, and differentiate into multinucleated placental bed giant cells. In addition, they can invade the maternal spiral arteries, mediate the destruction of the arterial wall, and replace the endothelium by forming endovascular trophoblasts [1,2]. * Correspondence: [email protected] † Equal contributors 1 Department of Obstetrics and Gynecology, College of Medicine, Catholic University, Seoul, Korea Full list of author information is available at the end of the article
During early pregnancy, the invasion of human trophoblast cells into the uterus is one of the essential events for the establishment of a successful pregnancy. It has been proposed that the processes by which placental cytotrophoblast cells change phenotypes from being coherently attached to being migratory, where cells inva
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