STAT3 and ERK Signaling Pathways Are Implicated in the Invasion Activity by Oncostatin M through Induction of Matrix Metalloproteinases 2 and 9 |
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| Authors: | Hyun Sun Ko Byung Joon Park Sae Kyung Choi Hee Kyung Kang Ahyoung Kim Ho Shik Kim In Yang Park Jong Chul Shin |
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| Affiliation: | 1Department of Obstetrics and Gynecology, College of Medicine, The Catholic University of Korea, Seoul, Korea.;2Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, Korea. |
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| Abstract: | PurposeOur previous studies have shown that oncostatin M (OSM) promotes trophoblast invasion activity through increased enzyme activity of matrix metalloproteinase (MMP)-2 and -9. We further investigated OSM-induced intracellular signaling mechanisms associated with these events in the immortalized human trophoblast cell line HTR8/SVneo.ResultsOSM-induced MMP-2 and -9 protein expression was significantly suppressed by STAT3 inhibition with stattic and STAT3 siRNA silencing, whereas the ERK1/2 inhibitor (U0126) and ERK silencing significantly suppressed OSM-induced MMP-2 protein expression. OSM-induced MMP-2 and MMP-9 enzymatic activities were significantly decreased by stattic pretreatment. The increased invasion activity induced by OSM was significantly suppressed by STAT3 and ERK1/2 inhibition, though to a greater extent by STAT3 inhibition.ConclusionBoth STAT3 and ERK signaling pathways are involved in OSM-induced invasion activity of HTR8/SVneo cells. Activation of STAT3 appears to be critical for the OSM-mediated increase in invasiveness of HTR8/SVneo cells. |
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