Met-HGF/SF mediates growth arrest and differentiation in T47D breast cancer cells

Dvora Ronen, Rom T. Altstock, Michal Firon, Leonid Mittelman, Tama Sobe, James H. Resau, George F. Vande Woude, Ilan Tsarfaty*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Hepatocyte growth factor/scatter factor (HGF/SF) is a pluripotent growth factor that exerts mitogenic, motogenic, and morphogenic effects. To elucidate the cellular mechanisms underlying the pluripotent function of this growth factor, T47D human breast cancer cells were transfected with human hgf/sf. The hgf/sf-positive clones exhibited different levels of biologically functional HGF/SF expression and up-regulation of endogenous Met (HGF/SF receptor) expression. In addition, a constitutive phosphorylation of the receptor on tyrosine residues was detected, establishing a Met-HGF/SF autocrine loop. The autocrine activation of Met caused marked inhibition in cell growth accompanied by cell accumulation at G0/G1. These cells underwent terminal cell differentiation as determined by morphological changes, synthesis of milk proteins such as β-casein and α-lactalbumin, and production of lipid vesicles. Our results demonstrate that Met-HGF/SF, an oncogenic signal transduction pathway, is capable of inducing growth arrest and differentiation in certain breast cancer cells and, thus, may have potential as therapeutic and/or prognostic tools in breast cancer treatment.

Original languageEnglish
Pages (from-to)131-140
Number of pages10
JournalCell Growth and Differentiation
Issue number2
StatePublished - Feb 1999


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