TY - JOUR
T1 - The role of TGF-β and its crosstalk with RAC1/RAC1b signaling in breast and pancreas carcinoma
AU - Melzer, Catharina
AU - Hass, Ralf
AU - von der Ohe, Juliane
AU - Lehnert, Hendrik
AU - Ungefroren, Hendrik
PY - 2017/5/12
Y1 - 2017/5/12
N2 - This article focusses on the role of TGF-β and its signaling crosstalk with the RHO family GTPases RAC1 and RAC1b in the progression of breast and pancreatic carcinoma. The aggressive nature of these tumor types is mainly due to metastatic dissemination. Metastasis is facilitated by desmoplasia, a peculiar tumor microenvironment and the ability of the tumor cells to undergo epithelial-mesenchymal transition (EMT) and to adopt a motile and invasive phenotype. These processes are controlled entirely or in part by TGF-β and the small RHO GTPase RAC1 with both proteins acting as tumor promoters in late-stage cancers. Data from our and other studies point to signaling crosstalk between TGF-β and RAC1 and the related isoform, RAC1b, in pancreatic and mammary carcinoma cells. Based on the exciting observation that RAC1b functions as an endogenous inhibitor of RAC1, we propose a model on how the relative abundance or activity of RAC1 and RAC1b in the tumor cells may determine their responses to TGF-β and, ultimately, the metastatic capacity of the tumor.
AB - This article focusses on the role of TGF-β and its signaling crosstalk with the RHO family GTPases RAC1 and RAC1b in the progression of breast and pancreatic carcinoma. The aggressive nature of these tumor types is mainly due to metastatic dissemination. Metastasis is facilitated by desmoplasia, a peculiar tumor microenvironment and the ability of the tumor cells to undergo epithelial-mesenchymal transition (EMT) and to adopt a motile and invasive phenotype. These processes are controlled entirely or in part by TGF-β and the small RHO GTPase RAC1 with both proteins acting as tumor promoters in late-stage cancers. Data from our and other studies point to signaling crosstalk between TGF-β and RAC1 and the related isoform, RAC1b, in pancreatic and mammary carcinoma cells. Based on the exciting observation that RAC1b functions as an endogenous inhibitor of RAC1, we propose a model on how the relative abundance or activity of RAC1 and RAC1b in the tumor cells may determine their responses to TGF-β and, ultimately, the metastatic capacity of the tumor.
UR - http://www.scopus.com/inward/record.url?scp=85025828488&partnerID=8YFLogxK
U2 - 10.1186/s12964-017-0175-0
DO - 10.1186/s12964-017-0175-0
M3 - Scientific review articles
C2 - 28499439
AN - SCOPUS:85025828488
SN - 1478-811X
VL - 15
JO - Cell communication and signaling : CCS
JF - Cell communication and signaling : CCS
IS - 1
ER -
