Expression of 14-3-3 sigma, cyclin-dependent kinases 2 and 4, p16, and Epstein–Barr nuclear antigen 1 in nasopharyngeal carcinoma

Huang, H. K.; Ch, Chen; Sc, Huang; Ch, Yang; Cf, Hwang

doi:10.1017/s0022215113003447

Cited by 4 publications

(3 citation statements)

References 28 publications

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“…In addition, it was demonstrated that the protein expression of CDKN2A was significantly decreased in C666-1 cells. Similarly, CDKN2A has been reported to be significantly downregulated in NPC tissues, and frequently methylated in the serum of patients with NPC (31,32). The results of the present study suggested that the decreased expression of CDKN2A may be caused by the upregulation of miR-663 in NPC.…”

Section: Discussionsupporting

confidence: 62%

miR-663 promotes NPC cell proliferation by directly targeting CDKN2A

Liang

Zhang

Deng

et al. 2017

Molecular Medicine Reports

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MicroRNAs (miRs) act as important regulators during the development and progression of human cancer; however, the regulatory mechanism of miR-663 in nasopharyngeal carcinoma (NPC) remains unclear. The present study demonstrated that serum miR‑663 levels were significantly increased in patients with NPC compared with healthy controls. In addition, the serum levels of miR‑663 were associated with the grade, lymph node metastasis and clinical stage of NPC. The expression of miR‑663 was increased in NPC C666‑1 cells, compared with normal nasopharyngeal epithelial NP69 cells. The knockdown of miR‑663 markedly decreased the proliferation of C666‑1 cells through the induction of cell cycle arrest at the G1 stage. Cyclin‑dependent kinase inhibitor 2A (CDKN2A) was hypothesized to be a putative target of miR‑663. Further investigation confirmed that miR‑663 was able to directly bind to the 3' untranslated region of CDKN2A mRNA, and to negatively regulate CDKN2A protein expression in C666‑1 cells. Inhibition of CDKN2A expression attenuated the suppressive effects of miR‑663 knockdown on the proliferation and cell cycle progression of C666‑1 cells. In addition, it was observed that the mRNA and protein levels of CDKN2A were decreased in C666‑1 cells compared with NP69 cells. In conclusion, the results of the present study demonstrated that miR‑663 promoted the proliferation and cell cycle progression of NPC cells by directly targeting CDKN2A, suggesting that miR‑663 may become a potential therapeutic target for the treatment of NPC.

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Section: Discussionsupporting

confidence: 62%

miR-663 promotes NPC cell proliferation by directly targeting CDKN2A

Liang

Zhang

Deng

et al. 2017

Molecular Medicine Reports

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“…Of the seven isoforms, 14-3-3σ is especially linked to cancer. Most of the isoforms are expressed in all tissues, whereas the σ isoform has been restricted to the epithelial cells (Wilker et al 2005;Huang et al 2014). 14-3-3σ is a protein kinase-dependent activator tyrosine and endogenous inhibitor of protein kinase C; it plays a negative role in the G2/M checkpoint, pausing the cell cycle and allowing DNA repair.…”

Section: Research Articlementioning

confidence: 99%

“…This work was supported by the Universidad de Las Palmas de Gran Canaria [grant number VD-IPD 2013-2014.…”

Section: Acknowledgementmentioning

confidence: 99%

Comparison of immunoreaction between two commercial antibodies against 14-3-3σprotein in canine tissues

Suárez‐Bonnet

Aguirre-Sanceledonio

Andrada

et al. 2015

Journal of Applied Animal Research

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Evaluation of 14-3-3 sigma as a potential partner of p16 in quiescence and differentiation

Agarwal

DeInnocentes

Bird

2018

In Vitro Cell.Dev.Biol.-Animal

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p16 is an important tumor suppressor gene encoded by the INK4A/ARF/INK4B gene locus that is conserved in humans, rodents, and canids. p16 regulates cell cycle in early G1 phase inhibiting transition out of cell cycle from G1/S phase by regulating a multi-protein control complex. p16-associated proteins, cyclin D, CDK4, and CDK6, experience expression level decreases or do not change during cell differentiation and quiescence in contrast to constant p16 expression in post-proliferative cell phases. We hypothesized that p16 has alternate binding partners, other than classical proliferation-associated proteins such as CDKs, in these post-proliferative cell phases. Using co-immunoprecipitation, we have identified 14-3-3σ as a potential alternate binding partner for p16 in quiescent post-proliferative canine mammary cancer cells. Additionally, expression of 14-3-3σ was maintained as fibroblasts exit cell cycle and differentiate to adipocytes simultaneously with continued expression of p16. Based on these results, we suggest that 14-3-3σ protein may be an alternative binding partner for p16 active during cell quiescence and may associate with p16 during cell differentiation.

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Expression of 14-3-3 sigma, cyclin-dependent kinases 2 and 4, p16, and Epstein–Barr nuclear antigen 1 in nasopharyngeal carcinoma

Abstract: Levels of cyclin-dependent kinase 2 and Epstein-Barr nuclear antigen 1 were significantly higher in nasopharyngeal carcinoma than in normal tissue, while p16 gene expression was diminished. These three proteins may contribute to nasopharyngeal carcinogenesis.

Cited by 4 publications

References 28 publications

miR-663 promotes NPC cell proliferation by directly targeting CDKN2A

miR-663 promotes NPC cell proliferation by directly targeting CDKN2A

Comparison of immunoreaction between two commercial antibodies against 14-3-3σprotein in canine tissues

Evaluation of 14-3-3 sigma as a potential partner of p16 in quiescence and differentiation

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