Transforming growth factor-beta, MAPK and Wnt signaling interactions in colorectal cancer

Harish R Cheruku; Abidali Mohamedali; David I Cantor; Sock-Hwee Tan; Edouard Nice; Mark S Baker

doi:10.1016/j.euprot.2015.06.004

Transforming growth factor-beta, MAPK and Wnt signaling interactions in colorectal cancer

Harish R Cheruku, Abidali Mohamedali, David I Cantor, Sock-Hwee Tan, Edouard Nice, Mark S Baker

Biochemistry & Molecular Biology

Research output: Contribution to journal › Article › Research › peer-review

29 Citations (Scopus)

Abstract

In non-cancerous cells, transforming growth factor-b (TGFb) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFb promotes tumoral growth via Smad-independent mechanisms and is involved in crosstalk with various pathways like the mitogen-activated protein kinases (MAPK) and Wnt. Crosstalk between these pathways following activation by TGFb and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFb signaling crosstalk involving various MAPK pathway members (e.g., extracellular signal-regulated kinase (Erk) 1/2, Ras, c-Jun N-terminal kinases (JNK) and p38) and the Wnt signaling pathway.

Original language	English
Pages (from-to)	104 - 115
Number of pages	12
Journal	EuPA Open Proteomics
Volume	8
DOIs	https://doi.org/10.1016/j.euprot.2015.06.004
Publication status	Published - 2015

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title = "Transforming growth factor-beta, MAPK and Wnt signaling interactions in colorectal cancer",

abstract = "In non-cancerous cells, transforming growth factor-b (TGFb) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFb promotes tumoral growth via Smad-independent mechanisms and is involved in crosstalk with various pathways like the mitogen-activated protein kinases (MAPK) and Wnt. Crosstalk between these pathways following activation by TGFb and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFb signaling crosstalk involving various MAPK pathway members (e.g., extracellular signal-regulated kinase (Erk) 1/2, Ras, c-Jun N-terminal kinases (JNK) and p38) and the Wnt signaling pathway.",

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T1 - Transforming growth factor-beta, MAPK and Wnt signaling interactions in colorectal cancer

AU - Cheruku, Harish R

AU - Mohamedali, Abidali

AU - Cantor, David I

AU - Tan, Sock-Hwee

AU - Nice, Edouard

AU - Baker, Mark S

PY - 2015

Y1 - 2015

N2 - In non-cancerous cells, transforming growth factor-b (TGFb) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFb promotes tumoral growth via Smad-independent mechanisms and is involved in crosstalk with various pathways like the mitogen-activated protein kinases (MAPK) and Wnt. Crosstalk between these pathways following activation by TGFb and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFb signaling crosstalk involving various MAPK pathway members (e.g., extracellular signal-regulated kinase (Erk) 1/2, Ras, c-Jun N-terminal kinases (JNK) and p38) and the Wnt signaling pathway.

AB - In non-cancerous cells, transforming growth factor-b (TGFb) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFb promotes tumoral growth via Smad-independent mechanisms and is involved in crosstalk with various pathways like the mitogen-activated protein kinases (MAPK) and Wnt. Crosstalk between these pathways following activation by TGFb and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFb signaling crosstalk involving various MAPK pathway members (e.g., extracellular signal-regulated kinase (Erk) 1/2, Ras, c-Jun N-terminal kinases (JNK) and p38) and the Wnt signaling pathway.

UR - http://www.sciencedirect.com/science/article/pii/S2212968515300064

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DO - 10.1016/j.euprot.2015.06.004

M3 - Article

SN - 2212-9685

VL - 8

SP - 104

EP - 115

JO - EuPA Open Proteomics

JF - EuPA Open Proteomics

ER -

Transforming growth factor-beta, MAPK and Wnt signaling interactions in colorectal cancer

Abstract

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