Silencing of ZRF1 impedes survival of estrogen receptor positive MCF-7 cells and potentiates the effect of curcumin View Full Text


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Article Info

DATE

2016-06-27

AUTHORS

Sandip Kumar Rath, Moonmoon Deb, Dipta Sengupta, Vijayalaxmi Kari, Swayamsiddha Kar, Sabnam Parbin, Nibedita Pradhan, Samir Kumar Patra

ABSTRACT

The role and clinical implication of ZRF1 in breast cancer are poorly understood. So this study is aimed to explore the role of ZRF1 in breast cancer progression. With this context, we first assessed its expression pattern in FFPE primary and metastasis breast tissue samples as well as from publicly available databases. Moreover, we also explored the survival status of patients from the publicly available database and interestingly discover that high expression of ZRF1 decreases the survival of estrogen-positive breast cancer patients more than estrogen-negative status patients. In the perspective of this, we evaluated the role ZRF1 in MCF-7 breast cancer cells and found that it’s silencing by knockdown results in decreased cell proliferation as well as cell viability. Results also show that expression of ZRF1 is down regulated in the presence of estrogen-depleted conditions but independent of RAS/MEK as well as AKT axes. Moreover, the decrease in viability of MCF-7 cells was accompanied by induction of apoptosis and DNA damage, well-marked with upregulation of cleaved PARP and downregulation of BCL2 and H2AUbK119 levels. Furthermore, we also explored that knockdown of ZRF1 sensitises the effect of curcumin, observed with decrease in cell viability and dropping of IC50 value from 25 to 15 μM. This investigation thus shed a new light on the role on ZRF1 in breast cancer cells and hence can be exploited to design better therapeutic intervention. More... »

PAGES

12535-12546

References to SciGraph publications

  • 2013-12-02. ZRF1 controls the retinoic acid pathway and regulates leukemogenic potential in acute myeloid leukemia in ONCOGENE
  • 2011-09-24. An improved non-enzymatic “DNA ladder assay” for more sensitive and early detection of apoptosis in CYTOTECHNOLOGY
  • 2006-06-27. The comet assay: a method to measure DNA damage in individual cells in NATURE PROTOCOLS
  • 2009-11-26. PARP inhibitors and the treatment of breast cancer: beyond BRCA1/2? in BREAST CANCER RESEARCH
  • 2014-09-06. Elucidation of caveolin 1 both as a tumor suppressor and metastasis promoter in light of epigenetic modulators in TUMOR BIOLOGY
  • 2014-07-29. Current and upcoming approaches to exploit the reversibility of epigenetic mutations in breast cancer in BREAST CANCER RESEARCH
  • 2014-10-13. Expression profiling of DNA methylation-mediated epigenetic gene-silencing factors in breast cancer in CLINICAL EPIGENETICS
  • 2010-12-22. Transcriptional activation of polycomb-repressed genes by ZRF1 in NATURE
  • 2006-12-21. Clonogenic assay of cells in vitro in NATURE PROTOCOLS
  • 2014-06-18. Optimizing Direct Immunofluorescence in HISTOPATHOLOGY
  • 2011-03-24. Cell Sensitivity Assays: The MTT Assay in CANCER CELL CULTURE
  • 2009-12-18. An online survival analysis tool to rapidly assess the effect of 22,277 genes on breast cancer prognosis using microarray data of 1,809 patients in BREAST CANCER RESEARCH AND TREATMENT
  • 2012-06-25. ZRF1 controls oncogene-induced senescence through the INK4-ARF locus in ONCOGENE
  • 2015-07-17. Poly(ADP-ribose) polymerase as a novel regulator of 17β-estradiol-induced cell growth through a control of the estrogen receptor/IGF-1 receptor/PDZK1 axis in JOURNAL OF TRANSLATIONAL MEDICINE
  • 2014-03-22. Functional conservation and divergence of J-domain-containing ZUO1/ZRF orthologs throughout evolution in PLANTA
  • 2010-12-17. Molecular marks for epigenetic identification of developmental and cancer stem cells in CLINICAL EPIGENETICS
  • 2005-05-02. Expression of estrogen receptor α, retinoic acid receptor α and cellular retinoic acid binding protein II genes is coordinately regulated in human breast cancer cells in ONCOGENE
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s13277-016-5114-y

    DOI

    http://dx.doi.org/10.1007/s13277-016-5114-y

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1031953928

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27350366


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    37 schema:description The role and clinical implication of ZRF1 in breast cancer are poorly understood. So this study is aimed to explore the role of ZRF1 in breast cancer progression. With this context, we first assessed its expression pattern in FFPE primary and metastasis breast tissue samples as well as from publicly available databases. Moreover, we also explored the survival status of patients from the publicly available database and interestingly discover that high expression of ZRF1 decreases the survival of estrogen-positive breast cancer patients more than estrogen-negative status patients. In the perspective of this, we evaluated the role ZRF1 in MCF-7 breast cancer cells and found that it’s silencing by knockdown results in decreased cell proliferation as well as cell viability. Results also show that expression of ZRF1 is down regulated in the presence of estrogen-depleted conditions but independent of RAS/MEK as well as AKT axes. Moreover, the decrease in viability of MCF-7 cells was accompanied by induction of apoptosis and DNA damage, well-marked with upregulation of cleaved PARP and downregulation of BCL2 and H2AUbK119 levels. Furthermore, we also explored that knockdown of ZRF1 sensitises the effect of curcumin, observed with decrease in cell viability and dropping of IC50 value from 25 to 15 μM. This investigation thus shed a new light on the role on ZRF1 in breast cancer cells and hence can be exploited to design better therapeutic intervention.
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