HRG/HER2/HER3 signaling promotes AhR-mediated Memo-1 expression and migration in colorectal cancer
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HRG/HER2/HER3 signaling promotes AhR-mediated Memo-1 expression and migration in colorectal cancer. / Bogoevska, V; Wolters-Eisfeld, G; Hofmann, B T; El Gammal, A T; Mercanoglu, B; Gebauer, F; Vashist, Y K; Bogoevski, D; Perez, D; Gagliani, N; Izbicki, J R; Bockhorn, M; Güngör, C.
In: ONCOGENE, Vol. 36, No. 17, 27.04.2017, p. 2394-2404.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - HRG/HER2/HER3 signaling promotes AhR-mediated Memo-1 expression and migration in colorectal cancer
AU - Bogoevska, V
AU - Wolters-Eisfeld, G
AU - Hofmann, B T
AU - El Gammal, A T
AU - Mercanoglu, B
AU - Gebauer, F
AU - Vashist, Y K
AU - Bogoevski, D
AU - Perez, D
AU - Gagliani, N
AU - Izbicki, J R
AU - Bockhorn, M
AU - Güngör, C
PY - 2017/4/27
Y1 - 2017/4/27
N2 - Colorectal cancer (CRC) is a complex disease with still unsatisfactory prognosis even in western societies, although substantial progress has been made in pre-screening programs, surgical techniques and targeted therapy options. Mediator of motility-1 (Memo-1) was previously recognized as an important effector of cell migration downstream of receptor tyrosine kinase signaling in breast cancer. This study identified Memo-1 as frequently overexpressed in CRC and established a close link between extracellular HER2 activation, AhR/ARNT transcriptional activity and Memo-1 expression. Dissection of the hMemo-1 gene promoter using reporter assays and chromatin IP techniques revealed recruitment of Aryl hydrocarbon receptor (AhR)/Aryl hydrocarbon receptor nuclear-translocator (ARNT) complex, which positively influenced Memo-1 expression in cancer cells. We found that Memo-1 depletion negatively influenced the cellular actin network and that its expression is required for HER2-mediated cell migration and invasion. Moreover, analyses of Memo-1 expression in primary CRC revealed correlation with clinical parameters that point to Memo-1 as a new prognostic factor of aggressive disease in CRC patients. Altogether, these observations demonstrate that Memo-1 is an important downstream regulator of HER2-driven CRC cell migration and invasion through connecting extracellular signals from membrane to the cytoskeletal actin network.Oncogene advance online publication, 12 December 2016; doi:10.1038/onc.2016.390.
AB - Colorectal cancer (CRC) is a complex disease with still unsatisfactory prognosis even in western societies, although substantial progress has been made in pre-screening programs, surgical techniques and targeted therapy options. Mediator of motility-1 (Memo-1) was previously recognized as an important effector of cell migration downstream of receptor tyrosine kinase signaling in breast cancer. This study identified Memo-1 as frequently overexpressed in CRC and established a close link between extracellular HER2 activation, AhR/ARNT transcriptional activity and Memo-1 expression. Dissection of the hMemo-1 gene promoter using reporter assays and chromatin IP techniques revealed recruitment of Aryl hydrocarbon receptor (AhR)/Aryl hydrocarbon receptor nuclear-translocator (ARNT) complex, which positively influenced Memo-1 expression in cancer cells. We found that Memo-1 depletion negatively influenced the cellular actin network and that its expression is required for HER2-mediated cell migration and invasion. Moreover, analyses of Memo-1 expression in primary CRC revealed correlation with clinical parameters that point to Memo-1 as a new prognostic factor of aggressive disease in CRC patients. Altogether, these observations demonstrate that Memo-1 is an important downstream regulator of HER2-driven CRC cell migration and invasion through connecting extracellular signals from membrane to the cytoskeletal actin network.Oncogene advance online publication, 12 December 2016; doi:10.1038/onc.2016.390.
U2 - 10.1038/onc.2016.390
DO - 10.1038/onc.2016.390
M3 - SCORING: Journal article
C2 - 27941874
VL - 36
SP - 2394
EP - 2404
JO - ONCOGENE
JF - ONCOGENE
SN - 0950-9232
IS - 17
ER -