Heightened Expression of CTCF in Breast Cancer Cells Is Associated with Resistance to Apoptosis

Farrar, Dawn; D'Arcy, Vivien; Chernukhin, Igor; Robinson, Alison; Loukinov, Dmitry; Vatolin, Sergei; Pack, Svetlana D.; Mackay, Alan; Harris, R. Adron; Dorricott, Heather; O’Hare, Michael J.; Lobanenkov, Victor; Klenova, Elena

doi:10.1158/0008-5472.can-03-3498

Cited by 93 publications

(110 citation statements)

References 45 publications

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“…Alterations involving CTCF may also be informative. Elevated CTCF expression levels have been reported in breast cancer, where it is postulated to have antiapoptotic actions [66]. Gene activation by a CTCF homolog is observed in lung cancer [67,68], and methylation changes in CTCF binding sites have also been reported in osteosarcoma [69].…”

Section: Loss Of Igf2 Imprintingmentioning

confidence: 99%

IGF2: Epigenetic regulation and role in development and disease

Chao

D'Amore

2008

Cytokine & Growth Factor Reviews

277

221

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Insulin-like growth factor II (IGF2) is perhaps the most intricately regulated of all growth factors characterized to date. Its gene is imprinted-only one allele is active, depending on parental origin -and this pattern of expression is maintained epigenetically in almost all tissues. IGF2 activity is further controlled through differential expression of receptors and IGF-binding proteins (IGFBPs) that determine protein availability. This complex and multifaceted regulation emphasizes the importance of accurate IGF2 expression and activity. This review will examine the regulation of the IGF2 gene and what it has revealed about the phenomenon of imprinting, which is frequently disrupted in cancer. IGF2 protein function will be discussed, along with diseases that involve IGF2 overexpression. Roles for IGF2 in sonic hedgehog (Shh) signaling and angiogenesis will also be explored.

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Section: Loss Of Igf2 Imprintingmentioning

confidence: 99%

IGF2: Epigenetic regulation and role in development and disease

Chao

D'Amore

2008

Cytokine & Growth Factor Reviews

277

221

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“…These results suggest that CTCF may be a determinant factor to death signaling pathways in these cells. However, other studies demonstrate contrary to the pro-apoptotic role of CTCF that knockdown and overexpression of CTCF in breast cancer cells result in triggering apoptosis and protecting ectopic expression of Bax-induced apoptosis, respectively [18]. In addition, CTCF expression levels are elevated in corneal epithelial cells in growth factor-induced proliferation [12].…”

Section: Introductionmentioning

confidence: 99%

Functional role of CCCTC binding factor (CTCF) in stress-induced apoptosis

2007

Experimental Cell Research

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CTCF, a nuclear transcriptional factor, is a multifunctional protein and involves regulation of growth factor-and cytokine-induced cell proliferation/differentiation. In the present study, we investigated the role of CTCF in protecting stress-induced apoptosis in various human cell types. We found that UV irradiation and hyper-osmotic stress induced human corneal epithelial (HCE) and hematopoietic myeloid cell apoptosis detected by significantly increased caspase 3 activity and decreased cell viability. The stress-induced apoptotic response in these cells requires down-regulation of CTCF at both mRNA and protein levels, suggesting that CTCF may play an important role in downstream events of stress-induced signaling pathways. Inhibition of NFκB activity prevented stress-induced down-regulation of CTCF and increased cell viability against stress-induced apoptosis. The antiapoptotic effect of CTCF was further studied by manipulating CTCF activities in HCE and hematopoietic cells. Transient transfection of cDNAs encoding full-length human CTCF markedly suppressed stress-induced apoptosis in these cells. In contrast, knocking down of CTCF mRNA using siRNA specific to CTCF significantly promoted stress-induced apoptosis. Thus, our results reveal that CTCF is a down stream target of stress-induced signaling cascades and it plays a significant antiapoptotic role in regulation of stress-induced cellular responses in HCE and hematopoietic myeloid cells.

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“…CTCF overexpression has been associated with growth suppression in different cellular systems; therefore, it is considered to be a tumor suppressor (Rasko et al, 2001;Rakha et al, 2004;Torrano et al, 2005;Docquier et al, 2005;Recillas-Targa et al, 2006;Ramli et al, 2012;Ouboussad et al, 2013). However, the opposite effect has been observed in other cell types (Heath et al, 2008); thus, it has been hypothesized that these differences in gene transcription and regulation of cell growth mediated by CTCF depend on the chromatin environment, transcriptional machinery, and metabolic state of different cell types .…”

Section: Discussionmentioning

confidence: 99%

BORIS and CTCF are overexpressed in squamous intraepithelial lesions and cervical cancer

Velázquez-Hernández¹,

Reyes-Romero²,

Barragán-Hernández³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We investigated the expression of Brother of Regulator of Imprinted Sites (BORIS) and CCCTC-binding factor (CTCF) in squamous intraepithelial lesions and cervical cancer. To analyze BORIS and CTCF expression, an endocervical cytobrush sample was taken for total RNA isolation. CTCF and BORIS mRNA was quantified from total RNA using quantitative reverse transcription-polymerase chain reaction. A total of 71 samples were collected and classified according to the Bethesda Classification of squamous intraepithelial lesions. BORIS 6095 BORIS and CTCF expression in cervical dysplasia and cancer ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 6094-6100 (2015) expression was observed in 9 (12.7%) samples; of these, 5.3, 5.9, 14.8, and 37.5% in the groups that were cytology negative for intraepithelial lesion or malignancy, low-grade squamous intraepithelial lesions (LSIL), highgrade squamous intraepithelial lesions (HSIL), and invasive cervical carcinoma, respectively. The expression level of BORIS was significantly higher in the group with invasive cervical carcinoma as compared with the groups negative for intraepithelial lesion or malignancy, LSIL, and HSIL (P < 0.0005). CTCF mRNA was expressed in all samples. CTCF expression was significantly higher in carcinoma groups compared with LSIL, HSIL, and negative for intraepithelial lesion or malignancy groups. We found that BORIS and CTCF expressions in the LSIL and invasive cervical carcinoma groups were higher than expression in cytological normal samples. Additional studies should be conducted to examine the function of transcription factors during different stages of the transformation of cervical cancer cells.

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Heightened Expression of CTCF in Breast Cancer Cells Is Associated with Resistance to Apoptosis

Cited by 93 publications

References 45 publications

IGF2: Epigenetic regulation and role in development and disease

IGF2: Epigenetic regulation and role in development and disease

Functional role of CCCTC binding factor (CTCF) in stress-induced apoptosis

BORIS and CTCF are overexpressed in squamous intraepithelial lesions and cervical cancer

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