scholarly journals Vaccinia-related kinase 1 (VRK1) confers resistance to DNA-damaging agents in human breast cancer by affecting DNA damage response

Oncotarget ◽  
2014 ◽  
Vol 5 (7) ◽  
pp. 1770-1778 ◽  
Author(s):  
Marcella Salzano ◽  
Marta Vázquez-Cedeira ◽  
Marta Sanz-García ◽  
Alberto Valbuena ◽  
Sandra Blanco ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Dna Damaging Agents ◽  
Damage Response

scholarly journals RAD50 targeting impairs DNA damage response and sensitizes human breast cancer cells to cisplatin therapy

2014 ◽  
Vol 15 (6) ◽  
pp. 777-788 ◽  
Author(s):  
Ali Flores-Pérez ◽  
Lourdes E Rafaelli ◽  
Nayeli Ramírez-Torres ◽  
Elena Aréchaga-Ocampo ◽  
Sara Frías ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Damage Response ◽  
Cisplatin Therapy

scholarly journals HSATII RNA is induced via a non-canonical ATM-regulated DNA-damage response pathway and facilitates tumor cell proliferation and movement

2020 ◽  
Author(s):  
Maciej T. Nogalski ◽  
Thomas Shenk
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Rna Expression ◽  
Tumor Cell Proliferation ◽  
Dna Damaging Agents ◽  
Damage Response ◽  
Infected Cells ◽  
Dna Damage Response Pathway

ABSTRACTPericentromeric human satellite II (HSATII) repeats are normally silent, but can be actively transcribed in tumor cells, where increased HSATII copy number is associated with a poor prognosis in colon cancer, and in human cytomegalovirus (HCMV)-infected cells, where the RNA facilitates viral replication. Here, we report that HCMV infection or treatment of ARPE-19 diploid epithelial cells with the DNA-damaging agents, etoposide and zeocin, induced HSATII RNA expression, and a kinase-independent function of ATM was required for the induction. Additionally, various breast cancer cell lines growing in adherent, 2-dimensional cell culture expressed HSATII RNA at different levels, and levels were markedly increased when cells were either infected with HCMV or treated with zeocin. High levels of HSATII RNA expression correlated with enhanced migration of breast cancer cells, and knockdown of HSATII RNA reduced cell migration and the rate of cell proliferation. Our investigation links high expression of HSATII RNA to the DNA damage response, centered on a non-canonical function of ATM, and demonstrates a role for the satellite RNA in tumor cell proliferation and movement.SIGNIFICANCEHSATII RNA is associated with cancer progression, immunostimulation and, as we recently reported, it plays an important role in herpesvirus infections. However, the understanding of cellular processes responsible for the expression of HSATII RNA has been limited. Our current investigation identified a non-canonical, ATM kinase-independent DNA-damage response pathway as a common cellular mechanism regulating HSATII RNA induction in virus-infected cells or cells treated with DNA-damaging agents. Additionally, our study provides a link between expression of HSATII RNA and the cellular growth and migration phenotypes of cancer cells, establishing a new paradigm to study the biological consequences of HSATII RNA expression, i.e., treatment of normal diploid and tumor cells with DNA-damaging agents.

scholarly journals Erratum: The mir-34 microRNA is required for the DNA damage response in vivo in C. elegans and in vitro in human breast cancer cells

Oncogene ◽  
2009 ◽  
Vol 28 (33) ◽  
pp. 3008-3008 ◽  
Author(s):  
M Kato ◽  
T Paranjape ◽  
R U Müller ◽  
S Nallur ◽  
E Gillespie ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage Response ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
C Elegans ◽  
Damage Response

scholarly journals HSATII RNA is induced via a noncanonical ATM-regulated DNA damage response pathway and promotes tumor cell proliferation and movement

2020 ◽  
Vol 117 (50) ◽  
pp. 31891-31901
Author(s):  
Maciej T. Nogalski ◽  
Thomas Shenk
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Tumor Cell ◽  
Dna Damage Response ◽  
Breast Cancer Cell Lines ◽  
Rna Expression ◽  
Tumor Cell Proliferation ◽  
Dna Damaging Agents ◽  
Damage Response

Pericentromeric human satellite II (HSATII) repeats are normally silent but can be actively transcribed in tumor cells, where increased HSATII copy number is associated with a poor prognosis in colon cancer, and in human cytomegalovirus (HCMV)-infected fibroblasts, where the RNA facilitates viral replication. Here, we report that HCMV infection or treatment of ARPE-19 diploid epithelial cells with DNA-damaging agents, etoposide or zeocin, induces HSATII RNA expression, and a kinase-independent function of ATM is required for the induction. Additionally, various breast cancer cell lines growing in adherent, two-dimensional cell culture express HSATII RNA at different levels, and levels are markedly increased when cells are infected with HCMV or treated with zeocin. High levels of HSATII RNA expression correlate with enhanced migration of breast cancer cells, and knockdown of HSATII RNA reduces cell migration and the rate of cell proliferation. Our investigation links high expression of HSATII RNA to the DNA damage response, centered on a noncanonical function of ATM, and demonstrates a role for the satellite RNA in tumor cell proliferation and movement.

scholarly journals The mir-34 microRNA is required for the DNA damage response in vivo in C. elegans and in vitro in human breast cancer cells

Oncogene ◽  
2009 ◽  
Vol 28 (25) ◽  
pp. 2419-2424 ◽  
Author(s):  
M Kato ◽  
T Paranjape ◽  
R Ullrich ◽  
S Nallur ◽  
E Gillespie ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage Response ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
C Elegans ◽  
Damage Response
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