Growth hormone enhances LNCaP prostate cancer cell motility

Abstract

Purpose: Prostate cancer cells are responsive to multiple hormones and growth factors that can affect cell function. These effects may include modulating cell proliferation and apoptosis, but the ability to impinge on the metastatic potential of prostate cancer cells by affecting cell motility should also be considered, as prostate tumor metastasis correlates with limited therapeutic options and poor prognosis. Human growth hormone (hGH) can affect the growth and survival of prostate cancer cells, but the effect of hGH on prostate cancer cell motility is unknown. In the present study, the potential for exogenous and autocrine hGH to directly affect prostate cancer cell motility was addressed. Materials and methods: The effects of exogenous and autocrine hGH on the chemokinesis and chemotaxis of LNCaP prostate cancer cells were tested using cell monolayer wound healing and Boyden chamber invasion assays. The signaling pathways underlying these effects were resolved with chemical inhibitors and the correlation with cytoskeletal actin reorganization evaluated microscopically by staining cells with fluor-conjugated phalloidin. Results: Both exogenous and autocrine hGH augmented the migration and invasion of LNCaP cells, and hGH itself acted as a chemoattractant. This activity was dependent upon the STAT5, MEK1/2 and PI3K signaling pathways, and was accompanied by an alteration in cellular actin organization. Conclusions: hGH may enhance the metastatic potential of prostate cancer cells, both as a stimulant of cellular motility and invasiveness and as a chemoattractant.

• Growth hormone
• prostate cancer
• metastasis
• motility
• signal transduction

Acknowledgements

The authors wish to thank Holly Jefferson for technical assistance.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. This work was supported by grants from the Leo W. Jenkins Cancer Center and the Brody Brothers Medical Foundation (#MT7749) to BMS.