Zinc finger proteins in cancer progression

Jen, Chauying J.; Wang, Yi‐Ching

doi:10.1186/s12929-016-0269-9

Cited by 290 publications

(243 citation statements)

References 100 publications

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“…Cellular zinc homeostasis is controlled by two families of zinc transporters with opposing actions, the ZnT family and the ZIP family . Dysregulation of zinc‐finger transcription factors and zinc transporters has been implicated in the progression of cancer . Specific to HCC, hepatoma cells have significantly lower intracellular zinc levels than normal hepatic cells, and the ZIP14 zinc transporter is markedly downregulated in the hepatoma cells .…”

Section: Discussionmentioning

confidence: 99%

“…The liver is responsible for production of carrier proteins for copper and zinc and is also the main site for copper storage, which plays a central role in maintaining copper and zinc homeostasis . A growing body of evidence has established a strong connection between the disruption of copper and/or zinc homeostasis and the development and progression of cancer . Data from case–control studies indicate higher copper levels, lower zinc levels, or higher copper/zinc ratio in patients with various cancers, including HCC .…”

Section: Introductionmentioning

confidence: 99%

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Serum copper and zinc levels at diagnosis and hepatocellular carcinoma survival in the Guangdong Liver Cancer Cohort

Fang

Chen

Wang

et al. 2019

Intl Journal of Cancer

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Copper and zinc are essential micronutrients, whose imbalance may be involved in the development and progression of cancer. However, the role of copper and/or zinc imbalance in the prognosis of hepatocellular carcinoma (HCC) is currently unclear. Our objective was to investigate the association between serum levels of copper, zinc and their ratio (copper/zinc) at diagnosis with HCC survival. We included 989 patients with incident HCC in this prospective cohort study, who were enrolled in the Guangdong Liver Cancer Cohort (GLCC) study within 30 days of diagnosis between September 2013 and February 2017. Serum copper and zinc were measured using inductively coupled plasma mass spectrometry. Primary outcomes were liver cancer‐specific survival (LCSS) and overall survival (OS). Cox proportional hazards models were used to calculate the multivariable hazard ratios (HRs) and 95% confidence interval (CI). Higher serum copper levels were strongly associated with worse LCSS (Q4 vs. Q1: HR = 1.87, 95% CI: 1.22–2.86; p < 0.01 for trend) and OS (Q4 vs. Q1: HR = 2.06, 95% CI: 1.36–3.11; p < 0.01 for trend). The calculated copper/zinc ratio was positively associated with LCSS (Q4 vs. Q1: HR = 1.31, 95% CI: 0.89–1.92; P = 0.04 for trend) and OS (Q4 vs. Q1: HR = 1.43, 95% CI: 0.99–2.08; P = 0.01 for trend). No overall associations were observed between serum zinc levels and LCSS or OS in the entire cohort. The results suggest that higher serum copper and copper in relation to zinc levels (i.e., higher copper/zinc ratio) may be associated with worse HCC survival, but serum zinc levels may be not associated with HCC survival.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Serum copper and zinc levels at diagnosis and hepatocellular carcinoma survival in the Guangdong Liver Cancer Cohort

Fang

Chen

Wang

et al. 2019

Intl Journal of Cancer

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“…GFI1 (Growth Factor Independent 1 Transcriptional Repressor) (4 sites) is a protein-coding gene, and its methylation was found to be the most robust mediator of the association between maternal smoking and birthweight in a recent study of children and newborns exposed to maternal and paternal smoking [47]. ZNF668 (2 sites) is a zinc finger protein whose role in DNA repair, cell proliferation and cancer has been investigated [48]. Chromosome region 1p36 (2 sites) has been investigated as a region containing a possible tumor suppressor [49]; with investigations including the effects of methylation [50].…”

Section: Discussionmentioning

confidence: 99%

The dynamics of smoking-related disturbed methylation: a two time-point study of methylation change in smokers, non-smokers and former smokers

et al. 2017

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Background: The evidence for epigenome-wide associations between smoking and DNA methylation continues to grow through cross-sectional studies. However, few large-scale investigations have explored the associations using observations for individuals at multiple time-points. Here, through the use of the Illumina 450K BeadChip and data collected at two time-points separated by approximately 7 years, we investigate changes in methylation over time associated with quitting smoking or remaining a former smoker, and those associated with continued smoking. Results: Our results indicate that after quitting smoking the most rapid reversion of altered methylation occurs within the first two decades, with reversion rates related to the initial differences in methylation. For 52 CpG sites, the change in methylation from baseline to follow-up is significantly different for former smokers relative to the change for never smokers (lowest p-value 3.61 x 10 -39 for cg26703534, gene AHRR). Most of these sites' respective regions have been previously implicated in smoking-associated diseases. Despite the early rapid change, dynamism of methylation appears greater in former smokers vs never smokers even four decades after cessation. Furthermore, our study reveals the heterogeneous effect of continued smoking: the methylation levels of some loci further diverge between smokers and non-smokers, while others re-approach. Though intensity of smoking habit appears more significant than duration, results remain inconclusive. Conclusions: This study improves the understanding of the dynamic link between cigarette smoking and methylation, revealing the continued fluctuation of methylation levels decades after smoking cessation and demonstrating that continuing smoking can have an array of effects. The results can facilitate insights into the molecular mechanisms behind smoking-induced disturbed methylation, improving the possibility for development of biomarkers of past smoking behavior and increasing the understanding of the molecular path from exposure to disease.

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“…Studies have shown that ZFX functions as a transcription factor [65] with the capacity to regulate self-renewal and cell survival in embryonic and haematopoietic stem cells [66,67]. ZFX has been recognised as an oncogene in a number of cancers (reviewed in [68]). In prostate cancer cell lines, ZFX has been shown to drive cell proliferation and promote cell survival [69] and expression of ZFX has been shown to be elevated in prostate tumours [69,70].…”

Section: Discussionmentioning

confidence: 99%

Genome-wide analysis of AR binding and comparison with transcript expression in primary human fetal prostate fibroblasts and cancer associated fibroblasts

Nash

Boufaied

Mills

et al. 2018

Molecular and Cellular Endocrinology

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Zinc finger proteins in cancer progression

Cited by 290 publications

References 100 publications

Serum copper and zinc levels at diagnosis and hepatocellular carcinoma survival in the Guangdong Liver Cancer Cohort

Serum copper and zinc levels at diagnosis and hepatocellular carcinoma survival in the Guangdong Liver Cancer Cohort

The dynamics of smoking-related disturbed methylation: a two time-point study of methylation change in smokers, non-smokers and former smokers

Genome-wide analysis of AR binding and comparison with transcript expression in primary human fetal prostate fibroblasts and cancer associated fibroblasts

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