Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis

Matteo Caforio, Cristina Sorino, Stefano Iacovelli, Maurizio Fanciulli, Franco Locatelli, Valentina Folgiero

Research output: Contribution to journalReview article

Abstract

BACKGROUND: The mechanism by which c-Myc exerts its oncogenic functions is not completely clear and different hypotheses are still under investigation. The knowledge of the capacity of c-Myc to bind exclusively E-box sequences determined the discrepancy between, on the one hand, genomic studies showing the binding of c-Myc to all active promoters and, on the other hand, the evidence that only 60% or less of the binding sites have E-box sequences.

MAIN BODY: In this review, we provide support to the hypothesis that the cooperation of c-Myc with transcriptional cofactors mediates c-Myc-induced cellular functions. We produce evidence that recently identified cofactors are involved in c-Myc control of survival mechanisms of cancer cells.

CONCLUSION: The identification of new c-Myc cofactors could favor the development of therapeutic strategies able to compensate the difficulty of targeting c-Myc.

Original languageEnglish
Pages (from-to)239
JournalJournal of Experimental and Clinical Cancer Research
Volume37
Issue number1
DOIs
Publication statusPublished - Sep 27 2018

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E-Box Elements
Carcinogenesis
Binding Sites
Neoplasms
Therapeutics

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Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis. / Caforio, Matteo; Sorino, Cristina; Iacovelli, Stefano; Fanciulli, Maurizio; Locatelli, Franco; Folgiero, Valentina.

In: Journal of Experimental and Clinical Cancer Research, Vol. 37, No. 1, 27.09.2018, p. 239.

Research output: Contribution to journalReview article

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AU - Caforio, Matteo

AU - Sorino, Cristina

AU - Iacovelli, Stefano

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AU - Locatelli, Franco

AU - Folgiero, Valentina

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N2 - BACKGROUND: The mechanism by which c-Myc exerts its oncogenic functions is not completely clear and different hypotheses are still under investigation. The knowledge of the capacity of c-Myc to bind exclusively E-box sequences determined the discrepancy between, on the one hand, genomic studies showing the binding of c-Myc to all active promoters and, on the other hand, the evidence that only 60% or less of the binding sites have E-box sequences.MAIN BODY: In this review, we provide support to the hypothesis that the cooperation of c-Myc with transcriptional cofactors mediates c-Myc-induced cellular functions. We produce evidence that recently identified cofactors are involved in c-Myc control of survival mechanisms of cancer cells.CONCLUSION: The identification of new c-Myc cofactors could favor the development of therapeutic strategies able to compensate the difficulty of targeting c-Myc.

AB - BACKGROUND: The mechanism by which c-Myc exerts its oncogenic functions is not completely clear and different hypotheses are still under investigation. The knowledge of the capacity of c-Myc to bind exclusively E-box sequences determined the discrepancy between, on the one hand, genomic studies showing the binding of c-Myc to all active promoters and, on the other hand, the evidence that only 60% or less of the binding sites have E-box sequences.MAIN BODY: In this review, we provide support to the hypothesis that the cooperation of c-Myc with transcriptional cofactors mediates c-Myc-induced cellular functions. We produce evidence that recently identified cofactors are involved in c-Myc control of survival mechanisms of cancer cells.CONCLUSION: The identification of new c-Myc cofactors could favor the development of therapeutic strategies able to compensate the difficulty of targeting c-Myc.

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