Please use this identifier to cite or link to this item: https://doi.org/10.3892/or.2011.1305
Title: Autocrine human growth hormone reduces mammary and endometrial carcinoma cell sensitivity to mitomycin C
Authors: Bougen, N.M.
Yang, T.
Chen, H.
Lobie, P.E. 
Perry, J.K.
Keywords: Chemotherapy
Drug resistance
Endometrial carcinoma
Growth hormone
Mammary carcinoma
Mitomycin C
Issue Date: Aug-2011
Citation: Bougen, N.M., Yang, T., Chen, H., Lobie, P.E., Perry, J.K. (2011-08). Autocrine human growth hormone reduces mammary and endometrial carcinoma cell sensitivity to mitomycin C. Oncology Reports 26 (2) : 487-493. ScholarBank@NUS Repository. https://doi.org/10.3892/or.2011.1305
Abstract: Drug resistance is a major cause of chemotherapy failure in breast cancer patients with metastatic disease. We previously demonstrated that autocrine human growth hormone (hGH) plays a key role in oncogenic transformation and progression of mammary carcinoma. The present study investigated the role of autocrine hGH in the development of resistance to mitomycin C (MMC), an alkylating agent utilised in the treatment of advanced metastatic breast cancer. Stable forced expression of the hGH gene was established in the mammary carcinoma cell lines MDA-MB-231, MCF-7 and T47D. Autocrine hGH reduced the sensitivity of mammary carcinoma cells to MMC in cell viability assays and reduced MMC-induced apoptotic cell death when compared to a control cell line. In addition, autocrine hGH enhanced MDA-MB-231 clonogenic survival, anchorage independent cell growth, growth in 3D Matrigel and protected MDA-MB-231 cells from induction of DNA double-strand breaks following MMC treatment. Functional antagonism of hGH in the endometrial carcinoma cell line RL95-2, which endogenously expresses hGH, significantly increased the sensitivity of these cells to MMC-induced DNA damage and cell death. Thus, autocrine hGH promotes mammary and endometrial carcinoma cell resistance to MMC. These studies indicate a potential role for antagonism of autocrine hGH in chemoresistant breast cancer.
Source Title: Oncology Reports
URI: http://scholarbank.nus.edu.sg/handle/10635/109208
ISSN: 1021335X
DOI: 10.3892/or.2011.1305
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