Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.24 (mitogen-activated protein kinase)
 95,810 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overexpression of transmembrane protease, serine 3 (TMPRSS3) has been detected in ovarian cancer. However, the molecular mechanisms of TMPRSS3 in ovarian cancer remain unclear. In the present study, we found that TMPRSS3 was significantly expressed in ovarian cancer cells. Overexpression of TMPRSS3 promoted the proliferation, invasion and migration of A2780 cells. Conversely, knockdown of TMPRSS3 in HO8910 cells inhibited the proliferation, invasion and migration. Furthermore, TMPRSS3 affected the expression levels of E-cadherin, vimentin and Twist. In addition, TMPRSS3 induced activation of ERK1/2 in ovarian cancer cells, and the ERK1/2 pathway was required for the TMPRSS3-mediated proliferation, invasion and migration of ovarian cancer cells. Finally, knockdown of TMPRSS3 inhibited ovarian cancer HO8910 cell growth and metastasis in vivo. Collectively, the present study suggests that TMPRSS3 plays a crucial role in the development and progression of ovarian cancer. Therefore, TMPRSS3 represents a potential therapeutic target of ovarian cancer.
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PMID:TMPRSS3 modulates ovarian cancer cell proliferation, invasion and metastasis. 2653 Oct 4

The transmembrane protease, serine 3 (TMPRSS3), a member of the type II transmembrane serine protease family, plays an important role in mediating tissue development, homeostasis and various biological processes. Recently, TMPRSS3 has been reported to be involved in cancer progression. However, the role of TMPRSS3 in gastric cancer (GC) remains largely unknown. In this study, we found that TMPRSS3 was highly expressed in GC tissues and cell lines. Knockdown of TMPRSS3 inhibited GC cell proliferation, invasion and epithelial-mesenchymal transition (EMT) in vitro as well as suppressed GC cell growth and dissemination in vivo. These inhibitory effects were mediated by regulation of the ERK1/2 signaling pathway. Moreover, TMPRSS3-mediated ERK1/2 activation was dependent on the PI3K/Akt pathway. In conclusion, TMPRSS3 contributed to GC progression via activation of the PI3K/Akt/ERK signaling pathway and might act as a therapeutic target for GC treatment.
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PMID:Knockdown of TMPRSS3 inhibits gastric cancer cell proliferation, invasion and EMT via regulation of the ERK1/2 and PI3K/Akt pathways. 3014 46