Semaphorins are mainly known as guidance signals in development, acting through receptors called Plexins. However, their role in cancer is rapidly emerging in the regulation of tumor angiogenesis, tumor growth, cancer cell invasiveness, and metastatic spreading. Intriguingly, activated plexins can transactivate receptor tyrosine kinases, such as MET, VEGFR2, FGFR2, and ERBB2, and lead to distinctive effects in a cell-context-dependent manner. Moreover, certain semaphorins concomitantly target endothelial and cancer cells, and can achieve remarkable inhibition of angiogenesis and tumor growth, associated with anti-metastatic activity. Altogether, these data validate the identification of semaphorin signals as promising therapeutic targets in cancer. © 2012 Elsevier Inc.

Tamagnone, L., Emerging Role of Semaphorins as Major Regulatory Signals and Potential Therapeutic Targets in Cancer, <<CANCER CELL>>, 2012; 22 (2): 145-152. [doi:10.1016/j.ccr.2012.06.031] [http://hdl.handle.net/10807/140950]

Emerging Role of Semaphorins as Major Regulatory Signals and Potential Therapeutic Targets in Cancer

Tamagnone, Luca
2012

Abstract

Semaphorins are mainly known as guidance signals in development, acting through receptors called Plexins. However, their role in cancer is rapidly emerging in the regulation of tumor angiogenesis, tumor growth, cancer cell invasiveness, and metastatic spreading. Intriguingly, activated plexins can transactivate receptor tyrosine kinases, such as MET, VEGFR2, FGFR2, and ERBB2, and lead to distinctive effects in a cell-context-dependent manner. Moreover, certain semaphorins concomitantly target endothelial and cancer cells, and can achieve remarkable inhibition of angiogenesis and tumor growth, associated with anti-metastatic activity. Altogether, these data validate the identification of semaphorin signals as promising therapeutic targets in cancer. © 2012 Elsevier Inc.
2012
Inglese
Tamagnone, L., Emerging Role of Semaphorins as Major Regulatory Signals and Potential Therapeutic Targets in Cancer, <<CANCER CELL>>, 2012; 22 (2): 145-152. [doi:10.1016/j.ccr.2012.06.031] [http://hdl.handle.net/10807/140950]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10807/140950
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