2011
DOI: 10.1038/onc.2011.339
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Abstract: Oncoprotein C-MYC is overexpressed in human metastatic melanomas and melanoma-derived cells where it is required for suppression of oncogene-induced senescence (OIS). The genetic events that maintain high levels of C-MYC in melanoma cells and their role in OIS are unknown. Here, we report that C-MYC in cells from several randomly chosen melanoma lines was up-regulated at the protein level, and largely due to the increased protein stability. Of all known regulators of C-MYC stability, levels of B56α subunit of … Show more

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Cited by 36 publications
(30 citation statements)
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References 48 publications
(70 reference statements)
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“…The strong expression of the MYC-stabilizing protein CIP2A and clinical association of its signature in basal-like and HER2 þ breast cancers identified in this study provides a novel, plausible explanation for the increased MYC protein levels and activity in these breast cancer subtypes. Association of MYC amplification and CIP2A expression in breast cancer is another novel finding of this study and suggests that inhibition of bidirectional positive feedback loop between MYC and CIP2A (Khanna et al, 2009;Mannava et al, 2011) could be an attractive therapeutic target in breast cancers in which these two oncogenic alterations exist. Moreover, it is plausible that further functional analysis of MYC-dependent CIP2A signature genes will reveal novel mechanisms by which these two oncoproteins together promote disease progression in basal-like and HER2 þ breast cancers.…”
Section: Discussionmentioning
confidence: 94%
“…The strong expression of the MYC-stabilizing protein CIP2A and clinical association of its signature in basal-like and HER2 þ breast cancers identified in this study provides a novel, plausible explanation for the increased MYC protein levels and activity in these breast cancer subtypes. Association of MYC amplification and CIP2A expression in breast cancer is another novel finding of this study and suggests that inhibition of bidirectional positive feedback loop between MYC and CIP2A (Khanna et al, 2009;Mannava et al, 2011) could be an attractive therapeutic target in breast cancers in which these two oncogenic alterations exist. Moreover, it is plausible that further functional analysis of MYC-dependent CIP2A signature genes will reveal novel mechanisms by which these two oncoproteins together promote disease progression in basal-like and HER2 þ breast cancers.…”
Section: Discussionmentioning
confidence: 94%
“…Lentiviral infection protocol was described previously. 50,51 All infected cells were briefly selected for resistance to puromycin and used in the described assays.…”
Section: Methodsmentioning
confidence: 99%
“…Different PP2A complexes regulate serine/ threonine phosphorylation of numerous cellular targets implicated in a variety of physiologic and cellular processes (48). Although the role of PP2A is not thus far widely studied in the context of senescence, the emerging evidence does indicate that certain PP2A complexes do promote senescence (49). Related to the role of PP2A in CIP2A-mediated senescence resistance, inhibition of the B55a subunit of PP2A was identified to promote stability of E2F1 phosphorylated on serine 364 and to prevent p53-induced downregulation of E2F1 (17).…”
Section: P21 Mediates P53-induced Senescencementioning
confidence: 99%