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Autocrine Human Growth Hormone Stimulates Oncogenicity of Endometrial Carcinoma Cells

Liggins Institute and National Research Centre for Growth and Development (V.P., J.K.P., K.M.M., M.D.M., P.E.L.) and Department of Molecular Medicine and Pathology (P.E.L.), Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland 1142, New Zealand; Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences (X.-J.K., S.-M.L., T.Z.), University of Science and Technology of China, Hefei, Anhui 230027, People’s Republic of China; and Department of Pathology (Z.-S.W.), Anhui Medical University, Hefei, Anhui 230032, People’s Republic of China

Address all correspondence and requests for reprints to: Peter E. Lobie M.D., Ph.D., The Liggins Institute, University of Auckland, 2–6 Park Avenue, Private Bag 92019 Auckland, New Zealand. E-mail: p.lobie{at}auckland.ac.nz; or Tao Zhu, Ph.D., Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, People’s Republic of China. E-mail: zhut{at}ustc.edu.cn.

Recent published data have demonstrated elevated levels of human GH (hGH) in endometriosis and endometrial adenocarcinoma. Herein, we demonstrate that autocrine production of hGH can enhance the in vitro and in vivo oncogenic potential of endometrial carcinoma cells. Forced expression of hGH in endometrial carcinoma cell lines RL95-2 and AN3 resulted in an increased total cell number through enhanced cell cycle progression and decreased apoptotic cell death. In addition, autocrine hGH expression in endometrial carcinoma cells promoted anchorage-independent growth and increased cell migration/invasion in vitro. In a xenograft model of human endometrial carcinoma, autocrine hGH enhanced tumor size and progression. Changes in endometrial carcinoma cell gene expression stimulated by autocrine hGH was consistent with the altered in vitro and in vivo behavior. Functional antagonism of hGH in wild-type RL95-2 cells significantly reduced cell proliferation, cell survival, and anchorage-independent cell growth. These studies demonstrate a functional role for autocrine hGH in the development and progression of endometrial carcinoma and indicate potential therapeutic relevance of hGH antagonism in the treatment of endometrial carcinoma.

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