Expression of the Epigenetic factor BORIS (CTCFL) in the Human Genome

Necochea-Campion, Rosalia de; Ghochikyan, Anahit; Josephs, Steven F.; Zacharias, Shelly; Woods, Erik J.; Karimi‐Busheri, Feridoun; Alexandrescu, Doru T; Chen, Chien-Shing; Agadjanyan, Michael G.; Carrier, Ewa

doi:10.1186/1479-5876-9-213

Cited by 29 publications

(22 citation statements)

References 62 publications

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“…An important question remains as to why BORIS expression is frequently activated in diverse cancer cells . BORIS expression is regulated by a complex combination of factors, including alternative promoter usage, repression by CTCF and p53, and DNA methylation of cis ‐regulatory elements .…”

Section: Discussionmentioning

confidence: 99%

“…BORIS is a member of the cancer‐testis antigen (CTA) family owing to its highly restricted expression in normal adult testis and expression in diverse tissues following neoplastic transformation. Aberrant BORIS expression has been detected in ∼70% of all primary tumors and cancer cell lines . BORIS can induce the expression of other CTAs in select cancers but not in others .…”

mentioning

confidence: 99%

“…A direct role for BORIS in neoplasia has not been clearly defined, notwithstanding its aberrant expression in cancer and ability to activate other CTAs . To date there has been insufficient experimental evidence to classify BORIS as a tumor suppressor or oncogene.…”

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confidence: 99%

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The cancer‐testis antigen BORIS phenocopies the tumor suppressor CTCF in normal and neoplastic cells

Tiffen

Bailey

Marshall

et al. 2013

Intl Journal of Cancer

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BORIS and CTCF are paralogous, multivalent 11-zinc finger transcription factors that play important roles in organizing higherorder chromatin architecture. BORIS is a cancer-testis antigen with a poorly defined function in cancer, although it has been hypothesized to exhibit oncogenic properties. CTCF, however, has been postulated as a candidate tumor suppressor. We collated the genetic lesions in BORIS and CTCF from multiple cancers identified using high-throughput genomics. In BORIS, nonsense and missense mutations are evenly distributed. In CTCF, recurrent mutations are mostly clustered in the conserved zinc finger domain and at residues critical for contacting DNA and zinc ion co-ordination. Three missense mutations are common to both proteins. We used an inducible lentivector to express wildtype BORIS or CTCF in primary cells and cancer cell lines in order to define their functional differences. Both BORIS and CTCF caused a significant decrease in cell proliferation and clonogenic capacity, without alteration of specific cell cycle phases. Both BORIS and CTCF conferred protective effects in primary cells and some cancer cells during UV damage-induced apoptosis. Using a bioluminescent MCF-7 orthotopic breast cancer model in vivo, we demonstrated that CTCF and BORIS suppressed breast cancer growth. These findings provide further evidence that CTCF behaves as a tumor suppressor, and show BORIS has a similar growth inhibitory effect in vitro and in vivo. Hence, acquired zinc finger mutations may disrupt these functions, thereby contributing to tumor growth and development.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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The cancer‐testis antigen BORIS phenocopies the tumor suppressor CTCF in normal and neoplastic cells

Tiffen

Bailey

Marshall

et al. 2013

Intl Journal of Cancer

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“…BORIS is considered to be an oncogene because its aberrant expression has been detected in ~70% of all primary tumors and cancer cell lines analyzed (de Necochea-Campion et al, 2011); however, the direct role of BORIS in the pathophysiology of neoplasia is not completely understood.…”

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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“…Presumably, the factors that drive differential splicing of the survivin gene come into play during transcription as multiple transcription initiation sites creating mRNA variants have not been identified for survivin, as they have for other important oncogenes, such as the epigenetic regulator BORIS[75]. The human genome contains a 15 kb copy of the survivin gene located on chromosome 17 q25[47; 76] and all splice variants appear to be derived from the same initial transcript.…”

Section: Regulation Of Survivin Differential Splicingmentioning

confidence: 99%

Clinico-pathologic relevance of Survivin splice variant expression in cancer

et al. 2013

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Survivin is a member of the inhibitor of apoptosis (IAP) family and has multifunctional properties that include aspects of proliferation, invasion and cell survival control. Survivin is a promising candidate for targeted cancer therapy as its expression is associated with poor clinical outcome, more aggressive clinico-pathologic features, and resistance to radiation and chemotherapy. In the present review the different properties of the Survivin splice variants are discussed and their activities correlated with different aspects of cancer cell biology, to include subcellular location. Special emphasis is placed on our current understanding of these Survivin splice variants influence on each other and on the phenotypic responses to therapy that they may control.

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Expression of the Epigenetic factor BORIS (CTCFL) in the Human Genome

Cited by 29 publications

References 62 publications

The cancer‐testis antigen BORIS phenocopies the tumor suppressor CTCF in normal and neoplastic cells

The cancer‐testis antigen BORIS phenocopies the tumor suppressor CTCF in normal and neoplastic cells

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

Clinico-pathologic relevance of Survivin splice variant expression in cancer

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