Hepsin inhibits the cell growth of endometrial cancer

Keiichiro Nakamura, Norio Takamoto, Fernando Abarzua, Atsushi Hongo, Junichi Kodama, Yasutomo Nasu, Hiromi Kumon, Yuji Hiramatsu

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Currently, several therapeutic approaches including surgery, chemotherapy, and radiation therapy are available for the treatment of endometrial cancer. However, endometrial cancer cells may survive, resulting in relapse of the disease, and ultimately causing demise of the patient. Hepsin is a cell surface-expressed chymotrypsin-like serine protease and a member of the family of type II transmembrane serine proteases. To date, little is known about its precise mechanisms of action. We investigated the biological functions and effects in vitro and in vivo of Hepsin, using endometrial cancer cell lines transfected with Hepsin. In stably transfected Ishikawa/Hepsin cell lines (Hepsin-10 and -12), we observed a significant inhibitory effect on cell growth in a monolayer culture system and in anchorage-independent cell growth in soft agar in vitro. Furthermore, in a xenograft model, growth inhibitory effects were observed when compared with the effects of mock-transfected cells used as a control. Overall, Hepsin showed potential inhibitory effects mediated by the induction of 14-3-3σ expression which leads to both cell cycle arrest at the G2/M phase through cyclin B and cyclin A and the p53-dependent pathway activated by increasing the level of Bak and reducing the level of Bcl-2 and Bcl-xL.

Original languageEnglish
Pages (from-to)389-397
Number of pages9
JournalInternational journal of molecular medicine
Volume22
Issue number3
DOIs
Publication statusPublished - Sep 2008

Keywords

  • Cell cycle
  • Endometrial cancer
  • Hepsin

ASJC Scopus subject areas

  • Genetics

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  • Cite this

    Nakamura, K., Takamoto, N., Abarzua, F., Hongo, A., Kodama, J., Nasu, Y., Kumon, H., & Hiramatsu, Y. (2008). Hepsin inhibits the cell growth of endometrial cancer. International journal of molecular medicine, 22(3), 389-397. https://doi.org/10.3892/ijmm_00000035