2013
DOI: 10.1073/pnas.1310432110
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Abstract: The tumor suppressor p16 INK4A inhibits formation of enzymatically active complexes of cyclin-dependent kinases 4 and 6 (CDK4/6) with D-type cyclins. Oncogenic stress induces p16 INK4A expression, which in turn triggers cellular senescence through activation of the retinoblastoma tumor suppressor. Subversion of oncogene-induced senescence is a key step during cancer development, and many tumors have lost p16 INK4A activity by mutation or epigenetic silencing. Human papillomavirus (HPV)-associated tumors expres… Show more

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Cited by 147 publications
(154 citation statements)
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References 46 publications
(59 reference statements)
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“…Following this protocol, we constructed TALE-DNMTs targeting 24-bp sequences within the CDKN2A promoter (20). The TALE-DNMT illustrated in Figure 1B ed in cervical cancers, and may be subject to aberrant regulatory mechanisms in these transformed cells (21,22). Thus, we hypothesized that a primary human cell line might be a more suitable system to study functionality at this particular target.…”
Section: Resultsmentioning
confidence: 99%
“…Following this protocol, we constructed TALE-DNMTs targeting 24-bp sequences within the CDKN2A promoter (20). The TALE-DNMT illustrated in Figure 1B ed in cervical cancers, and may be subject to aberrant regulatory mechanisms in these transformed cells (21,22). Thus, we hypothesized that a primary human cell line might be a more suitable system to study functionality at this particular target.…”
Section: Resultsmentioning
confidence: 99%
“…INK4A depletion (25). Whereas the existing data suggest that p16 INK4A may favor proliferation and survival through more than one molecular mechanism, e.g., inhibition of cdk4 activity versus regulation of E7 expression, future studies are warranted to more precisely define potential interactions between the two pathways.…”
mentioning
confidence: 99%
“…The cellular function of p16 has been recently identified. Knock out of p16 in HPV E7 expressing cells can lead to induction of apoptosis showing a physiological role in transformation despite its original role in the process of senescence (39)(40)(41)(42). In another study inactivation of the p16 promotor by methylation has been shown (43).…”
Section: Discussionmentioning
confidence: 97%