Resistance to transforming growth factor β-mediated tumor suppression in melanoma: are multiple mechanisms in place?

Carcinogenesis
Ahmed Lasfar, Karine Cohen-Solal

Abstract

Resistance to transforming growth factor (TGF) β-mediated tumor suppression in melanoma appears to be a crucial step in tumor aggressiveness since it is usually coupled with the ability of TGFβ to drive the oncogenic process via autocrine and paracrine effects. In this review, we will focus mainly on the mechanisms of escape from TGFβ-induced cell cycle arrest because the mechanisms of resistance to TGFβ-mediated apoptosis are still essentially speculative. As expected, some of these mechanisms can directly affect the function of the main downstream effectors of TGFβ, Smad2 and Smad3, resulting in compromised Smad-mediated antiproliferative activity. Other mechanisms can counteract or overcome TGFβ-mediated cell cycle arrest independently of the Smads. In melanoma, some models of resistance to TGFβ have been suggested and will be described. In addition, we propose additional models of resistance taking into consideration the information available on the dysregulation of fundamental cellular effectors and signaling pathways in melanoma.

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Citations

Feb 7, 2012·Carcinogenesis·Jens WulfängerBarbara Seliger
Dec 23, 2011·Clinical & Developmental Immunology·Ahmed LasfarKarine A Cohen-Solal
Jan 28, 2014·Clinical and Translational Medicine·Simona RomanoMaria Fiammetta Romano
May 18, 2011·Oncogene·M I RodríguezF J Oliver
May 30, 2013·Annals of Dermatology·Carole Yolande PerrotAlain Mauviel
Mar 25, 2014·Cancer Letters·Rajeev K BoregowdaKarine A Cohen-Solal
Jun 16, 2011·British Journal of Cancer·S BraigA-K Bosserhoff
Oct 21, 2016·Oncotarget·Daniela D'ArcangeloAntonio Facchiano
Aug 7, 2018·World Journal of Stem Cells·Maria Teresa ValentiMonica Mottes
May 16, 2012·Cancer Discovery·James D Watson

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