BORIS up-regulates OCT4 via histone methylation to promote cancer stem cell-like properties in human liver cancer cells

Liu, Qiuying; Chen, Kefei; Liu, Zhong‐Jian; Huang, Yuan; Zhao, Rongzhen; Wei, Ling; Yu, Xiaoqin; He, Jingjing; Li, Jun; Qi, Jian-Guo; Qin, Yang; Li, Bo

doi:10.1016/j.canlet.2017.06.017

Cited by 40 publications

(51 citation statements)

References 42 publications

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“…Our observation that BORIS-expressing melanoma cells have increased migratory and invasive abilities are in agreement with previous studies that demonstrated that BORIS overexpression promoted EMT in liver cancer cell lines (25) as well as the CD44/CD133 positive subpopulation of the IMR-32 neuroblastoma cell line (65). However, in contrast, Alberti et al, revealed that BORIS knockdown promotes EMT in MCF7 breast cancer cells (66).…”

Section: Discussionsupporting

confidence: 93%

“…Our finding that altered BORIS expression leads to large-scale changes in gene expression was expected, as BORIS is known to act as a transcriptional regulator (24,25,29,33). In addition, it reflects the numerous cellular processes that BORIS is involved in (42,53), many of which are altered during carcinogenesis.…”

Section: Discussionsupporting

confidence: 60%

“…Brother of Regulator of Imprinted Sites (BORIS) is a DNA binding protein with high similarity to CCCTC binding factor (CTCF) (19), a multifunctional transcription factor that plays an important role in genome organization (20). In contrast to the tumor suppressive functions reported for CTCF (21,22), multiple studies have indicated an oncogenic role for BORIS (23)(24)(25)(26)(27). Like CTCF, BORIS plays a role in transcriptional regulation (24,25,28,29).…”

Section: Introductionmentioning

confidence: 99%

“…In contrast to the tumor suppressive functions reported for CTCF (21,22), multiple studies have indicated an oncogenic role for BORIS (23)(24)(25)(26)(27). Like CTCF, BORIS plays a role in transcriptional regulation (24,25,28,29). The mechanisms through which BORIS can alter transcription rely on BORIS' ability to bind the DNA at specific binding motifs, which are often found near promoter regions (30)(31)(32).…”

Section: Introductionmentioning

confidence: 99%

“…At these binding motifs BORIS can compete with DNA-bound CTCF (32), form a BORIS-CTCF heterodimer, or occupy a so-called BORIS-only binding site (31). Via these mechanisms BORIS can alter transcription by acting as a transcriptional activator (24,25,29,33), recruiting a transcriptional activator (34), altering DNA methylation (24,35,36) or histone modifications (24,28,29,35), or recruiting chromatin modifying proteins (37,38). In addition, it is believed that BORIS impacts the transcriptional landscape by interfering with CTCF-mediated chromatin loops (31,39).…”

Section: Introductionmentioning

confidence: 99%

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BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

Janssen

Moscona

Elchebly³

et al. 2019

Preprint

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Melanoma is among the most aggressive cancers due to its tendency to metastasize early. Phenotype switching between a proliferative and an invasive state has been suggested as a critical process for metastasis. The mechanisms that regulate these transitions are complex and remain poorly understood. Brother of Regulator of Imprinted Sites (BORIS), also known as CCCTC binding factor-Like (CTCFL), is a transcriptional modulator that becomes aberrantly expressed in melanoma. Here, we show that BORIS is involved in phenotype switching in melanoma. Genetic modification of BORIS expression in melanoma cells combined with whole transcriptome analysis indicated that BORIS expression contributes to an invasion-associated transcriptome. In agreement with this finding, inducible BORIS overexpression in melanoma cells reduced proliferation and increased migration and invasion, demonstrating that the transcriptional switch is accompanied by a phenotypic switch. Overall, our study indicates a pro-invasive role for BORIS in melanoma via transcriptional reprogramming.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

Janssen

Moscona

Elchebly³

et al. 2019

Preprint

View full text Add to dashboard Cite

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AMD1 upregulates hepatocellular carcinoma cells stemness by FTO mediated mRNA demethylation

Bian

Shi

Xing

et al. 2021

Clinical & Translational Med

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A genetic variant in the promoter of CD46 is associated with the risk and prognosis of hepatocellular carcinoma

Liu

Luo

Liu

et al. 2020

Molecular Carcinogenesis

Self Cite

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CD46 (also known as membrane cofactor protein), which is a member of the membrane-bound complement regulatory protein family, has been reported to cause cancer cells to escape complement-dependent cytotoxicity. However, the association between CD46 polymorphisms and the risk of hepatocellular carcinoma (HCC) has not been investigated. This two-stage association study was conducted to assess the relationship between the tagging single nucleotide polymorphisms (tagSNPs) of CD46 and HCC risk and prognosis. A series of functional analyses were performed to study the underlying mechanisms. Among the eight tagSNPs, rs2796267 (P = .003) and rs2796268 (P = .011) were found to modify HCC risk in the discovery set. Only rs2796267 (P < .0001) was confirmed to be associated with HCC susceptibility in the validation set. Compared with the wild-type AA genotype, the GG genotype significantly increased the HCC risk (adjusted odds ratio [OR] = 2.03; 95% confidence interval [CI], 1.34-3.08; P = .001). Moreover, subgroups analysis suggested a positive correlation among male and younger patients, especially among drinkers, smokers, and hepatitis B surface antigen-positive individuals. In functional analyses, we found that the rs2796267 G allele in the promoter region of CD46 could increase the expression of CD46 by affecting the binding affinity of STAT5a. Furthermore, Cox regression analysis revealed that the rs2796267 AG/GG genotype was significantly associated with worse prognosis of resected patients with HCC (hazard ratio = 2.27; 95% CI, 1.27-4.05; P = .006). These results suggest that the CD46 rs2796267 polymorphism may contribute to susceptibility and prognosis of HCC by altering promoter activity.

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BORIS up-regulates OCT4 via histone methylation to promote cancer stem cell-like properties in human liver cancer cells

Cited by 40 publications

References 42 publications

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

AMD1 upregulates hepatocellular carcinoma cells stemness by FTO mediated mRNA demethylation

A genetic variant in the promoter of CD46 is associated with the risk and prognosis of hepatocellular carcinoma

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