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 language | English |
|---|---|
| Pages (from-to) | 239 |
| Journal | Journal of Experimental and Clinical Cancer Research |
| Volume | 37 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Sep 27 2018 |
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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 journal › Review article
}
TY - JOUR
T1 - Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis
AU - Caforio, Matteo
AU - Sorino, Cristina
AU - Iacovelli, Stefano
AU - Fanciulli, Maurizio
AU - Locatelli, Franco
AU - Folgiero, Valentina
PY - 2018/9/27
Y1 - 2018/9/27
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.
U2 - 10.1186/s13046-018-0912-2
DO - 10.1186/s13046-018-0912-2
M3 - Review article
C2 - 30261904
VL - 37
SP - 239
JO - Journal of Experimental and Clinical Cancer Research
JF - Journal of Experimental and Clinical Cancer Research
SN - 0392-9078
IS - 1
ER -