scholarly journals DNA Repair by Homologous Recombination, But Not by Nonhomologous End Joining, Is Elevated in Breast Cancer Cells

Neoplasia ◽  
2009 ◽  
Vol 11 (7) ◽  
pp. 683-IN3 ◽  
Author(s):  
Zhiyong Mao ◽  
Ying Jiang ◽  
Xiang Liu ◽  
Andrei Seluanov ◽  
Vera Gorbunova
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Homologous Recombination ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Nonhomologous End Joining ◽  
End Joining

scholarly journals Survivin contributes to DNA repair by homologous recombination in breast cancer cells

2015 ◽  
Vol 155 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Eloïse Véquaud ◽  
Grégoire Desplanques ◽  
Pascal Jézéquel ◽  
Philippe Juin ◽  
Sophie Barillé-Nion
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Homologous Recombination ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals MiR223-3p promotes synthetic lethality in BRCA1-deficient cancers

2019 ◽  
Vol 116 (35) ◽  
pp. 17438-17443 ◽  
Author(s):  
Gayathri Srinivasan ◽  
Elizabeth A. Williamson ◽  
Kimi Kong ◽  
Aruna S. Jaiswal ◽  
Guangcun Huang ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cancer Cells ◽  
Synthetic Lethality ◽  
Negative Regulator ◽  
Nonhomologous End Joining ◽  
Chromosomal Translocations ◽  
Replication Forks ◽  
Repair Pathway ◽  
End Joining ◽  
Parp1 Inhibitors

Defects in DNA repair give rise to genomic instability, leading to neoplasia. Cancer cells defective in one DNA repair pathway can become reliant on remaining repair pathways for survival and proliferation. This attribute of cancer cells can be exploited therapeutically, by inhibiting the remaining repair pathway, a process termed synthetic lethality. This process underlies the mechanism of the Poly-ADP ribose polymerase-1 (PARP1) inhibitors in clinical use, which target BRCA1 deficient cancers, which is indispensable for homologous recombination (HR) DNA repair. HR is the major repair pathway for stressed replication forks, but when BRCA1 is deficient, stressed forks are repaired by back-up pathways such as alternative nonhomologous end-joining (aNHEJ). Unlike HR, aNHEJ is nonconservative, and can mediate chromosomal translocations. In this study we have found that miR223-3p decreases expression of PARP1, CtIP, and Pso4, each of which are aNHEJ components. In most cells, high levels of microRNA (miR) 223–3p repress aNHEJ, decreasing the risk of chromosomal translocations. Deletion of the miR223 locus in mice increases PARP1 levels in hematopoietic cells and enhances their risk of unprovoked chromosomal translocations. We also discovered that cancer cells deficient in BRCA1 or its obligate partner BRCA1-Associated Protein-1 (BAP1) routinely repress miR223-3p to permit repair of stressed replication forks via aNHEJ. Reconstituting the expression of miR223-3p in BRCA1- and BAP1-deficient cancer cells results in reduced repair of stressed replication forks and synthetic lethality. Thus, miR223-3p is a negative regulator of the aNHEJ DNA repair and represents a therapeutic pathway for BRCA1- or BAP1-deficient cancers.

scholarly journals Valproic acid causes radiosensitivity of breast cancer cells via disrupting the DNA repair pathway

2016 ◽  
Vol 5 (3) ◽  
pp. 859-870 ◽  
Author(s):  
Yue Luo ◽  
Hui Wang ◽  
Xipeng Zhao ◽  
Chao Dong ◽  
Fengmei Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Valproic Acid ◽  
Dna Repair ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Breast Cancer Cells ◽  
Histone Deacetylase Inhibitors ◽  
Clinical Treatment ◽  
Repair Pathway ◽  
Treatment Of Epilepsy

Valproic acid (VPA) is one of the representative compounds of histone deacetylase inhibitors (HDACis) and is used widely for the clinical treatment of epilepsy and other convulsive diseases.

scholarly journals Coordination of Centrosome Homeostasis and DNA Repair Is Intact in MCF-7 and Disrupted in MDA-MB 231 Breast Cancer Cells

2010 ◽  
Vol 70 (8) ◽  
pp. 3320-3328 ◽  
Author(s):  
Ilie D. Acu ◽  
Tieju Liu ◽  
Kelly Suino-Powell ◽  
Steven M. Mooney ◽  
Antonino B. D'Assoro ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Repair ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mcf 7

scholarly journals Molecular and Clinical Significance of Stanniocalcin-1 Expression in Breast Cancer Through Promotion of Homologous Recombination-Mediated DNA Damage Repair

2021 ◽  
Vol 9 ◽  
Author(s):  
Jing Hou ◽  
Jigan Cheng ◽  
ZeHua Dai ◽  
Na Wei ◽  
Huan Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Homologous Recombination ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Dna Damage Repair ◽  
Breast Cancer Cell Lines ◽  
Enzyme Linked Immunosorbent Assay ◽  
Glycoprotein Hormone ◽  
Damage Repair

Stanniocalcin-1 (STC1) is a glycoprotein hormone whose abnormal expression has been reported to be associated with a variety of tumors, but its function in breast cancer is not well understood. Through modulation of STC1 expression in different breast cancer cell lines, our study found that STC1 could promote the proliferation and growth of breast cancer cells and promote metastasis. Furthermore, STC1 reduced apoptosis induction by irradiation. We also found that STC1 could promote a homologous recombination-mediated DNA damage repair by recruiting BRCA1 to sites of damage. Moreover, STC1 silencing sensitized breast cancer cells to treatment with irradiation (IR), olaparib, or cisplatin in vitro. In clinical settings, the serum concentration of STC1 was higher in breast cancer patients than in healthy women, as detected by enzyme-linked immunosorbent assay (ELISA). In addition, immunohistochemical staining of breast cancer specimens showed that a high expression of STC1 was negatively correlated with recurrence-free survival in breast cancer, indicating that STC1 expression could be used as a predictive marker for a poor prognosis in breast cancer. All these findings indicate that STC1 promotes breast cancer tumorigenesis and that breast cancers with a high level of STC1 are more resistant to treatment, probably through homologous recombination (HR) promotion. Furthermore, combining STC1 inhibition and DNA damage-inducing drugs may be a novel approach to improve the survival of patients with STC1-expressing breast cancer.

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