Cyclin D1 and cyclin D-dependent kinases enhance oral keratinocyte proliferation but do not block keratinocyte differentiation

Woods, Michael C.; Pant, Rima; Mallya, Sanjay M.

doi:10.3892/ijo_00000799

Cited by 6 publications

(4 citation statements)

References 21 publications

(24 reference statements)

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“…This discrepancy in results is partly explained by the use of different histologic criteria for determining cyclin D1 expression. Another explanation was provided by Woods and colleagues in a study of oral keratinocyte cell lines in which stimulation of cyclin D1 expression increased cell proliferation but did not block cell differentiation [ 59 ]. This suggests that cyclin D1 is able to directly affect transcriptional regulation of genes involved in oral keratinocyte differentiation independently of CDK.…”

Section: Discussionmentioning

confidence: 99%

Nuclear Epidermal Growth Factor Receptor Overexpression as a Survival Predictor in Oral Squamous Cell Carcinoma

Tarle

Raguž

Müller

et al. 2023

IJMS

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The aim of this study was to determine, by immunohistochemical methods, the expression of nEGFR and markers of cell proliferation (Ki-67), cell cycle (mEGFR, p53, cyclin D1), and tumor stem cells (ABCG2) in 59 pathohistological samples of healthy oral mucosa, 50 oral premalignant changes (leukoplakia and erythroplakia), and 52 oral squamous cell carcinomas (OSCC). An increase in the expression of mEGFR and nEGFR was found with the development of the disease (p < 0.0001). In the group of patients with leukoplakia and erythroplakia, we found a positive correlation between nEGFR and Ki67, p53, cyclin D1, and mEGFR, whereas in the group of patients with OSCC, we found a positive correlation between nEGFR and Ki67, mEGFR (p < 0.05). Tumors without perineural (PNI) invasion had a higher expression of p53 protein than tumors with PNI (p = 0.02). Patients with OSCC and overexpression of nEGFR had shorter overall survival (p = 0.004). The results of this study suggest a potentially important independent role of nEGFR in oral carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Nuclear Epidermal Growth Factor Receptor Overexpression as a Survival Predictor in Oral Squamous Cell Carcinoma

Tarle

Raguž

Müller

et al. 2023

IJMS

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“…In an attempt to identify cellular proteins involved in cell cycle control which may be affected by the expression of HPV20E6, we investigated cyclin-D1, cdk6, p16 INK4a , PP2A and pRB. Cyclin-D1 and ckd6 enhance keratinocyte proliferation by phosphorylation of down-stream targets including pRB [60] , [61] . The increased pLXSN-flagHPV20E6 proliferation may be a consequence of increased expression of cell cycle proteins indirectly induced by HPV20E6 expression.…”

Section: Discussionmentioning

confidence: 99%

Differential Regulation of Cutaneous Oncoprotein HPVE6 by wtp53, Mutant p53R248W and ΔNp63α is HPV Type Dependent

Fei

Villiers

2012

PLoS ONE

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UV exposure and p53 mutations are major factors in non-melanoma skin cancer, whereas a role for HPV infections has not been defined. Previous data demonstrated the wtp53-mediated degradation of cutaneous HPV20E6 by caspase-3. ΔNp63α and hot-spot mutant p53R248W conveyed a protective effect on HPV20E6 under these conditions. We demonstrate a differential regulation by wtp53 of the E6 genes of cutaneous types HPV4, HPV5, HPV7, HPV27, HPV38, HPV48, HPV60 and HPV77. Caspase- or proteasome-mediated down-regulation was HPV type dependent. Mutant p53R248W up-regulated expression of all these E6 proteins as did ΔNp63α except for HPV38E6 which was down-regulated by the latter. None of these cellular proteins affected HPV41E6 expression. Ectopic expression of both mutp53R248W and ΔNp63α in the normal NIKS keratinocyte cell line harbouring endogenous p53 and p63however led to a down-regulation of HPV20E6. We demonstrate that HPV20E6 expression in these cells is modulated by additional, yet unidentified, cellular protein(s), which are not necessarily involved in apoptosis or autophagy. We further demonstrate proliferation of HPV20E6-expressing keratinocytes. Levels of proteins involved in cell cycle control, cyclin-D1, cdk6 and p16INK4a, phosphorylated pRB, as well as c-Jun and p-c-Jun, were all increased in these cells. HPV20E6 did not compete for the interaction between p16INK4a with cyclin-D1 or cdk6. Phosphorylation of pRB in the HPV20E6 expressing cells seems to be sufficient to override the cytokenetic block induced by the p16INK4a/pRB pathway. The present study demonstrates the diverse influence of p53 family members on individual cutaneous HPVE6 proteins. HPV20E6 expression also resulted in varying protein levels of factors involved in proliferation and differentiation.

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“…The recombinant LV encoded SOCS1 as well as EGFP. All recombinant lentiviruses were produced through transient transfection of the human embryonic kidney cell line (293T) according to standard protocols [16]. Viruses were concentrated by ultracentrifugation, aliquoted, and stored at -80 °C.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of Suppressors of Cytokine Signaling 1 Promotes the Neuronal Differentiation of C17.2 Neural Stem Cells

Cui

Dai²,

Xin³

et al. 2014

Cell Physiol Biochem

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Objective: To investigate the role and mechanism of suppressor of cytokine signaling 1 (SOCS1) in the regulation and differentiation of C17.2 neural stem cells (NSCs). Methods: In this study, lentiviral (LV)-SOCS1-enhanced green fluorescent protein (EGFP) was constructed and transfected into C17.2 NSCs. There were three groups of C17.2 NSCs: LV-SOCS1-EGFP, LV-EGFP, and phosphate-buffered saline (PBS). The expression levels of microtubule-associated protein 2 (MAP2), glial fibrillary acidic protein (GFAP), myelin basic protein (MBP), nestin, and β-tubulin III in C17.2 NSCs were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), immunocytochemistry, and western blot. In addition, the phosphorylation level of Jaks/Stats family members in C17.2 NSCs were analyzed by western blot. Moreover, the morphological changes of C17.2 NSCs after transfection were observed by light microscopy. Results: The gene expression of MAP2 increased significantly and the gene expression of nestin decreased significantly in C17.2 NSCs transfected with LV-SOCS1-EGFP. Some C17.2 NSCs underwent prominent neuronal morphological changes and expressed β-tubulin III after LV-SOCS1-EGFP transfection. The number of positive cells for β-tubulin III immunocytochemical staining and β-tubulin III protein expression in C17.2 NSCs after LV-SOCS1-EGFP transfection were both more than those after LV-EGFP transfection or PBS treatment. The phosphorylation levels of Jak2 and Stat3 but not Jak3 in C17.2 NSCs were inhibited by SOCS1 overexpression. Conclusion: Overexpression of SOCS1 in C17.2 NSCs promotes the generation of neurons, which is likely mediated by the negative feedback inhibition of Jak2 and Stat3. This study is the first to provide evidence that SOCS1 is involved in the regulation of neurogenesis.

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Cyclin D1 and cyclin D-dependent kinases enhance oral keratinocyte proliferation but do not block keratinocyte differentiation

Cited by 6 publications

References 21 publications

Nuclear Epidermal Growth Factor Receptor Overexpression as a Survival Predictor in Oral Squamous Cell Carcinoma

Nuclear Epidermal Growth Factor Receptor Overexpression as a Survival Predictor in Oral Squamous Cell Carcinoma

Differential Regulation of Cutaneous Oncoprotein HPVE6 by wtp53, Mutant p53R248W and ΔNp63α is HPV Type Dependent

Overexpression of Suppressors of Cytokine Signaling 1 Promotes the Neuronal Differentiation of C17.2 Neural Stem Cells

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