Cyclin D1 and P16 expression in recurrent nasopharyngeal carcinoma

Lin, Ho‐Sheng; Berry, Gerald J.; Sun, Zijie; Fee, Willard E.

doi:10.1016/s0194-5998(03)00770-8

Cited by 4 publications

(5 citation statements)

References 7 publications

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“…3). Further studies showed that protein level of cyclin D1, a protein which is frequent amplifiable and altered expression in a variety of tumors including NPC (Lamb and Ewen, 2003;Lin et al, 2006), decreased markedly by metformin treatment (Fig. 4).…”

Section: Discussionmentioning

confidence: 94%

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

Zhao

Wen

Jia

et al. 2011

The Anatomical Record

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It has been reported that metformin, a biguanide derivative widely used in type II diabetic patients, has antitumor activities in some cancers by activation of AMP-activated protein kinase (AMPK). But its role in nasopharyngeal carcinoma (NPC) is not known. Here, we reported for the first time that 1-50 mM of metformin in a dose-and time-dependent manner suppressed cell proliferation and colony formation in NPC cell line, C666-1. Further studies revealed that the protein level of cyclin D1 decreased and the percentage of the cells in G0/G1 phase increased by 5 mM metformin treatment. Metformin also induced the phosphorylation of AMPK (T172) in a time-dependent manner. Mammalian target of rapamycin complex 1 (mTORC1), which is negatively regulated by AMPK and plays a central role in cell growth and proliferation, was inhibited by metformin, as manifested by dephosphorylation of its downstream targets 40S ribosomal S6 kinase 1 (S6K1) (T389), the eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1) (T37/46) and S6 (S235/236) in C666-1 cells. In a summary, metformin prevents proliferation of C666-1 cells by down-regulating cyclin D1 level and inducing G1 cell cycle arrest. AMPK-mediated inhibition of mTORC1 signaling may be involved in this process. Anat Rec, 294:1337Rec, 294: -1343Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 94%

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

Zhao

Wen

Jia

et al. 2011

The Anatomical Record

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“…The second reason could be due to the concept of "minimal residual disease" theory, which postulates that histologically undetectable tumor deposits may remain at the primary site after initial treatment; which remain biologically dormant and only manifest overt disease after a period of time. 44 It is possible that these inert cells regain dominance through acquisition of new mutations because genetic mutations among patients with recurrent NPC, such as in p16, 45 fibulin-5, 46 and FLJ10540 47 have been reported. Alternatively, recurrent cancer may acquire qualities that enhance the ability of the tumor to evade the host immune system.…”

Section: Discussionmentioning

confidence: 99%

“…44 It is possible that these inert cells regain dominance through acquisition of new mutations because genetic mutations among patients with recurrent NPC, such as in p16, 45 fibulin-5, 46 and FLJ10540 47 have been reported. Alternatively, recurrent cancer may acquire qualities that enhance the ability of the tumor to evade the host immune system.…”

mentioning

confidence: 99%

Relapse status as a prognostic factor in patients receiving salvage surgery for recurrent or residual nasopharyngeal cancer after definitive treatment

et al. 2016

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“…Some authors have reported a correlation of altered F-12 staining with worse patient outcome in lung cancer [22], although others found no such correlation [23]. Moreover, it has been reported that p16INK4a inactivation, assessed with F-12 antibody, was involved in development and progression of other malignancies such as nasopharyngeal carcinoma [24], thick melanomas [25], and adrenocortical tumours [26]. While we can not eliminate that this antibody did bind to an isoform of the human p16INK4a protein in our tests or in the previously reported studies, further investigations are required before the reported F-12 data can be attributed with certainty to the human p16INK4a protein.…”

Section: Discussionmentioning

confidence: 99%

The Specificity and Patterns of Staining in Human Cells and Tissues of p16INK4a Antibodies Demonstrate Variant Antigen Binding

et al. 2013

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The validity of the identification and classification of human cancer using antibodies to detect biomarker proteins depends upon antibody specificity. Antibodies that bind to the tumour-suppressor protein p16INK4a are widely used for cancer diagnosis and research. In this study we examined the specificity of four commercially available anti-p16INK4a antibodies in four immunological applications. The antibodies H-156 and JC8 detected the same 16 kDa protein in western blot and immunoprecipitation tests, whereas the antibody F-12 did not detect any protein in western blot analysis or capture a protein that could be recognised by the H-156 antibody. In immunocytochemistry tests, the antibodies JC8 and H-156 detected a predominately cytoplasmic localised antigen, whose signal was depleted in p16INK4a siRNA experiments. F-12, in contrast, detected a predominately nuclear located antigen and there was no noticeable reduction in this signal after siRNA knockdown. Furthermore in immunohistochemistry tests, F-12 generated a different pattern of staining compared to the JC8 and E6H4 antibodies. These results demonstrate that three out of four commercially available p16INK4a antibodies are specific to, and indicate a mainly cytoplasmic localisation for, the p16INK4a protein. The F-12 antibody, which has been widely used in previous studies, gave different results to the other antibodies and did not demonstrate specificity to human p16INK4a. This work emphasizes the importance of the validation of commercial antibodies, aside to the previously reported use, for the full verification of immunoreaction specificity.

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Cyclin D1 and P16 expression in recurrent nasopharyngeal carcinoma

Cited by 4 publications

References 7 publications

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

Metformin Induces G1 Cell Cycle Arrest and Inhibits Cell Proliferation in Nasopharyngeal Carcinoma Cells

Relapse status as a prognostic factor in patients receiving salvage surgery for recurrent or residual nasopharyngeal cancer after definitive treatment

The Specificity and Patterns of Staining in Human Cells and Tissues of p16INK4a Antibodies Demonstrate Variant Antigen Binding

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