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

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

doi:10.1016/j.euprot.2015.06.004

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

Harish R. Cheruku, Abidali Mohamedali, David I. Cantor, Sock Hwee Tan, Edouard C. Nice, Mark S. Baker^*

^*Corresponding author for this work

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Abstract

In non-cancerous cells, transforming growth factor-β (TGFβ) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFβ 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 TGFβ and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFβ 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 - 1 Sept 2015

Bibliographical note

Copyright the Author(s) 2015. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

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

abstract = "In non-cancerous cells, transforming growth factor-β (TGFβ) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFβ 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 TGFβ and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFβ 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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note = "Copyright the Author(s) 2015. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.",

year = "2015",

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doi = "10.1016/j.euprot.2015.06.004",

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AU - Cheruku, Harish R.

AU - Mohamedali, Abidali

AU - Cantor, David I.

AU - Tan, Sock Hwee

AU - Nice, Edouard C.

AU - Baker, Mark S.

N1 - Copyright the Author(s) 2015. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

PY - 2015/9/1

Y1 - 2015/9/1

N2 - In non-cancerous cells, transforming growth factor-β (TGFβ) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFβ 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 TGFβ and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFβ 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-β (TGFβ) regulates cellular responses primarily through Smad signaling. However, during cancer progression (including colorectal) TGFβ 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 TGFβ and subsequent downstream signaling activity can be referred to as a crosstalk signaling signature. This review highlights the progress in understanding TGFβ 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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ER -

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

Abstract

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