Role of CTCF poly(ADP-Ribosyl)ation in the regulation of apoptosis in breast cancer cells

Bhooma Venkatraman*, Elena Klenova

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    3 Citations (Scopus)


    Introduction: CTCF is a candidate tumor suppressor gene encoding a multifunctional transcription factor. CTCF function is controlled by posttranslational modification and interaction with other proteins. Research findings suggested that CTCF function can be regulated by poly(ADP-ribosyl)ation (PARlation) and has specific anti-apoptotic function in breast cancer cells. The aim of this study is to assess the effect of CTCF-wild type (WT) and CTCF complete mutant, which is deficient of PARlation in regulating apoptosis in breast cancer cells. Materials and Methods: The effect of CTCF-WT and CTCF complete mutant was expressed in breast cancer cell-lines by DNA-mediated transfection technique monitored by enhanced green fluorescent protein fluorescence. Evaluation of apoptotic cell death was carried out with immunohistochemical staining using 4′-6′-diamino-2 phenylindole and scoring by fluorescent microscopy. Results: CTCF-WT supports survival of breast cancer cells and was observed that CTCF complete mutant interferes with the functions of the CTCF-WT and there was a considerable apoptotic cell death in the breast cancer cell lines such as MDA-MB-435, CAMA-1 and MCF-7. Conclusion: The study enlighten CTCF as a "Biological Marker" for breast cancer and the role of CTCF PARlation may be involved in breast carcinogenesis.

    Original languageEnglish
    Pages (from-to)49-54
    Number of pages6
    JournalIndian Journal of Medical and Paediatric Oncology
    Issue number1
    Publication statusPublished - 27 Mar 2015


    • 4′-6′-diamino-2 phenylindole
    • CTCF complete mutant
    • CTCF-wild type
    • poly(ADP-ribosyl)ation
    • transfection


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