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Tumor Suppressor Gene p16/INK4A Dependent Regulation of Cell Cycle Exit in a Spontaneous Canine Model of Breast Cancer Tumor Suppressor Gene p16/INK4A Dependent Regulation of Cell Cycle Exit in a Spontaneous Canine Model of Breast Cancer


Metadata FieldValueLanguage
dc.contributorbirdric@auburn.eduen_US
dc.creatorAgarwal, Payal
dc.creatorSandey, Maninder
dc.creatorDeInnocentes, Patricia
dc.creatorBird, R. Curtis
dc.date.accessioned2022-04-13T18:51:44Z
dc.date.available2022-04-13T18:51:44Z
dc.date.created2013
dc.identifier10.1002/jcb.24476en_US
dc.identifier.urihttps://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.24476en_US
dc.identifier.urihttps://aurora.auburn.edu/handle/11200/50060
dc.identifier.urihttp://dx.doi.org/10.35099/aurora-129
dc.description.abstract16/INK4A/CDKN2A is an important tumor suppressor gene that arrests cell cycle in G1 phase inhibiting binding of CDK4/6 with cyclin D1,leaving the Rb tumor suppressor protein unphosphorylated and E2F bound and inactive. We hypothesized that p16 has a role in exit from cellcycle that becomes defective in cancer cells. Well characterized p16-defective canine mammary cancer cell lines (CMT28, CMT27, andCMT12), derived stably p16-transfected CMT cell clones (CMT27A, CMT27H, CMT28A, and CMT28F), and normal canine fibroblasts (NCF),were used to investigate expression of p16 after serum starvation into quiescence followed by re-feeding to induce cell cycle re-entry. Theparental CMT cell lines used lack p16 expression either at the mRNA or protein expression levels, while p27 and other p16-associated proteins,including CDK4, CDK6, cyclin D1, and Rb, were expressed. We have successfully demonstrated cell cycle arrest and relatively synchronous cellcycle re-entry in parental CMT12, CMT28 and NCF cells as well as p16 transfected CMT27A, CMT27H, CMT28A, and CMT28F cells andconfirmed this by3H-thymidine incorporation and flow cytometric analysis of cell cycle phase distribution. p16-transfected CMT27A andCMT27H cells exited cell cycle post-serum-starvation in contrast to parental CMT27 cells. NCF, CMT27A, and CMT28F cells expressedupregulated levels of p27 and p16 mRNA, post-serum starvation, as cells exited cell cycle and entered quiescence. Because quiescence anddifferentiation are associated with increased levels of p27, our data demonstrating that p16 was upregulated along with p27 duringquiescence, suggests a potential role for p16 in maintaining these non-proliferative states.en_US
dc.formatPDFen_US
dc.publisherWiley Periodicals, LLCen_US
dc.relation.ispartofJournal of Cellular Biochemistryen_US
dc.relation.ispartofseries1097-4644en_US
dc.rights© 2012 This is the version of record published by Wiley Periodicals, Inc and is made available under the CC-BY-NC-ND 4.0 license. Item should be cited as: J Cell Biochem. 2013 Jun;114(6):1355-63. doi: 10.1002/jcb.24476. Tumor suppressor gene p16/INK4A/CDKN2A-dependent regulation into and out of the cell cycle in a spontaneous canine model of breast cancer Payal Agarwal 1, Maninder Sandey, Patricia DeInnocentes, R Curtis BirdSubmitted: First published: 13 December 2012 https://doi.org/10.1002/jcb.24476en_US
dc.subjectCANINE MAMMARY CANCER; BREAST CANCER; CELL QUIESCENCE; CELL CYCLen_US
dc.subjectcanine mammary canceren_US
dc.subjectbreast canceren_US
dc.subjectcell quiescenceen_US
dc.titleTumor Suppressor Gene p16/INK4A Dependent Regulation of Cell Cycle Exit in a Spontaneous Canine Model of Breast Cancer Tumor Suppressor Gene p16/INK4A Dependent Regulation of Cell Cycle Exit in a Spontaneous Canine Model of Breast Canceren_US
dc.typeTexten_US
dc.type.genreJournal Article, Academic Journalen_US
dc.citation.volume114en_US
dc.citation.issue6en_US
dc.citation.spage1355en_US
dc.citation.epage1363en_US
dc.description.statusPublisheden_US
dc.description.peerreviewyesen_US

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