KERATINOCYTE GROWTH FACTOR STIMULATES THE MIGRATION AND PROLIFERATION OF BREAST CANCER CELLS IN A CULTURE WOUNDING MODEL

• Published in: Pharmacological research 2002-08, Vol.46 (2), p.179-183
• Main Authors: NGUYEN, THAO-NGUYEN, ZANG, XIAO-PING, PENTO, J.THOMAS
• Format: Article
• Language: English
• Subjects: breast cancer cells; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Cell Culture Techniques; Cell Division - drug effects; cell migration; Cell Movement - drug effects; Dose-Response Relationship, Drug; Fibroblast Growth Factor 7; Fibroblast Growth Factors - metabolism; Fibroblast Growth Factors - pharmacology; Humans; in vitro wound model; keratinocyte growth factor; Neoplasm Invasiveness; Receptors, Estrogen - metabolism; Recombinant Proteins - metabolism; Recombinant Proteins - pharmacology; Time Factors; Tumor Cells, Cultured
• ISSN: 1043-6618; 1096-1186
• DOI: 10.1016/S1043-6618(02)00085-3

Growth factors are known to influence the progression, motility and invasiveness of tumor cells. In a previous study, we reported that conditioned media from NIH 3T3 cells (mouse fibroblast), which contains KGF, increased the motile morphology of estrogen receptor (ER)-positive breast cancer cells and produced no effect on ER-negative cells. The present study examined the influence of human KGF on two estrogen receptor (ER)-positive human breast cancer cell lines (MCF-7 and T-47D) using a culture wounding model to evaluate cell proliferation and migration over a period of 48 h. In the present study we observed that KGF enhanced the migration and proliferation of both MCF-7 and T-47D breast cancer cells. In both cell lines the response to KGF was found to be both dose- and time-dependent. However, the total migration and proliferation response of the MCF-7 cells to KGF was much greater than that observed in the T-47D cells. The results of this study demonstrate that human KGF enhances the migration and proliferation of human breast cancer cells. Further, these results support the concept that KGF may be an early signal in the progression of breast cancer to a more motile and metastatic phenotype.