2017
DOI: 10.3892/or.2017.5463
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Epigenetic activation of WHSC1 functions as an oncogene and is associated with poor prognosis in cervical cancer

Abstract: Overexpression of Wolf-Hirschhorn syndrome candidate 1 (WHSC1) is commonly observed in various types of tumors. However, the potential mechanism responsible for this molecular event is poorly understood. In the present study, we found that the mRNA levels of WHSC1 were significantly increased in cervical cancer cells, and that CpG sites were almost fully methylated in HaCaT cells, but partially methylated in HeLa and C33A cells. Clinically, the results of quantitative methylation-specific PCR (QMSP) and quanti… Show more

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Cited by 20 publications
(17 citation statements)
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“…Additionally, WHSC1 upregulation was positively correlated with the FIGO stage and differentiation, suggesting that WHSC1 might be a possible novel biomarker for poor prognosis of CC. Our results were consistent with those of other studies 16…”
Section: Discussionsupporting
confidence: 94%
“…Additionally, WHSC1 upregulation was positively correlated with the FIGO stage and differentiation, suggesting that WHSC1 might be a possible novel biomarker for poor prognosis of CC. Our results were consistent with those of other studies 16…”
Section: Discussionsupporting
confidence: 94%
“…In addition to the described genes, we can individually identify WHSC1, PRDM14 and ANXA11 genes which are involved in autoimmune disorders and in some cancers [ 50 52 ]. The set of functions governed by the genes selected and described has shown a particularly active state of the fibroblasts belonging to the subset of common metaMGUS and metaMM genes but without the adoption of a phenotype that can alter the bone marrow.…”
Section: Resultsmentioning
confidence: 99%
“…57 In agreement with Wu, Yin et al have shown that up-regulation of NSD2 significantly promotes the proliferation, migration, and invasion of cancer cells, and the underlying mechanism may be attributed to the activation of the AKT/metalloproteinase-2 (MMP-2) signaling pathway upon over-expression of NSD2. 58 Zhu et al have confirmed that the growth of cancer cells is reduced after depletion of NSD2 in vivo and in vitro. Meanwhile, cancer metastasis is inhibited through the regulation of TGF-1 (transforming growth factor-1)/TGF-RI/SMAD signaling pathway.…”
Section: Introductionmentioning
confidence: 93%
“…Previous studies have reported that NSD2 is over-expressed in the cervical cancer cells and tissues and associated with unfavorable prognosis. 57 , 58 Wu et al have displayed that a high level of NSD2 is associated with differentiation and stage, depletion of NSD2 inhibits cell proliferation, migration, and invasion, and this is affected by endothelial nitric oxide synthase (eNOS) signaling pathway. 57 In agreement with Wu, Yin et al have shown that up-regulation of NSD2 significantly promotes the proliferation, migration, and invasion of cancer cells, and the underlying mechanism may be attributed to the activation of the AKT/metalloproteinase-2 (MMP-2) signaling pathway upon over-expression of NSD2.…”
Section: Introductionmentioning
confidence: 99%