scholarly journals Berberine attenuates XRCC1‐mediated base excision repair and sensitizes breast cancer cells to the chemotherapeutic drugs

2019 ◽  
Vol 23 (10) ◽  
pp. 6797-6804 ◽  
Author(s):  
Xingjie Gao ◽  
Jing Wang ◽  
Meiqi Li ◽  
Jia Wang ◽  
Jian Lv ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Base Excision Repair ◽  
Breast Cancer Cells ◽  
Excision Repair ◽  
Chemotherapeutic Drugs ◽  
Base Excision

Chk1 inhibitor synergizes quinacrine mediated apoptosis in breast cancer cells by compromising the base excision repair cascade

2016 ◽  
Vol 105 ◽  
pp. 23-33 ◽  
Author(s):  
Ranjan Preet ◽  
Sumit Siddharth ◽  
Shakti Ranjan Satapathy ◽  
Sarita Das ◽  
Anmada Nayak ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Base Excision Repair ◽  
Breast Cancer Cells ◽  
Excision Repair ◽  
Chk1 Inhibitor ◽  
Base Excision

scholarly journals Author response: Perturbation of base excision repair sensitizes breast cancer cells to APOBEC3 deaminase-mediated mutations

2019 ◽  
Author(s):  
Birong Shen ◽  
Joseph H Chapman ◽  
Michael F Custance ◽  
Gianna M Tricola ◽  
Charles E Jones ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Base Excision Repair ◽  
Breast Cancer Cells ◽  
Excision Repair ◽  
Author Response ◽  
Base Excision

scholarly journals Perturbation of base excision repair sensitizes breast cancer cells to APOBEC3 deaminase-mediated mutations

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Birong Shen ◽  
Joseph H Chapman ◽  
Michael F Custance ◽  
Gianna M Tricola ◽  
Charles E Jones ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Base Excision Repair ◽  
Breast Cancer Cells ◽  
Excision Repair ◽  
Entry Site ◽  
Abasic Sites ◽  
Elevated Expression ◽  
Base Excision

Abundant APOBEC3 (A3) deaminase-mediated mutations can dominate the mutational landscape (‘mutator phenotype’) of some cancers, however, the basis of this sporadic vulnerability is unknown. We show here that elevated expression of the bifunctional DNA glycosylase, NEIL2, sensitizes breast cancer cells to A3B-mediated mutations and double-strand breaks (DSBs) by perturbing canonical base excision repair (BER). NEIL2 usurps the canonical lyase, APE1, at abasic sites in a purified BER system, rendering them poor substrates for polymerase β. However, the nicked NEIL2 product can serve as an entry site for Exo1 in vitro to generate single-stranded DNA, which would be susceptible to both A3B and DSBs. As NEIL2 or Exo1 depletion mitigates the DNA damage caused by A3B expression, we suggest that aberrant NEIL2 expression can explain certain instances of A3B-mediated mutations.

scholarly journals GSK-3β Can Regulate the Sensitivity of MIA-PaCa-2 Pancreatic and MCF-7 Breast Cancer Cells to Chemotherapeutic Drugs, Targeted Therapeutics and Nutraceuticals

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 816
Author(s):  
Stephen L. Abrams ◽  
Shaw M. Akula ◽  
Akshaya K. Meher ◽  
Linda S. Steelman ◽  
Agnieszka Gizak ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Cancer Cells ◽  
Mitochondrial Respiration ◽  
Breast Cancer Cells ◽  
Chemotherapeutic Drugs ◽  
Pancreatic Cancers ◽  
Signal Transduction Inhibitors ◽  
Gsk 3Β ◽  
Mcf 7

Glycogen synthase kinase-3 (GSK-3) is a regulator of signaling pathways. KRas is frequently mutated in pancreatic cancers. The growth of certain pancreatic cancers is KRas-dependent and can be suppressed by GSK-3 inhibitors, documenting a link between KRas and GSK-3. To further elucidate the roles of GSK-3β in drug-resistance, we transfected KRas-dependent MIA-PaCa-2 pancreatic cells with wild-type (WT) and kinase-dead (KD) forms of GSK-3β. Transfection of MIA-PaCa-2 cells with WT-GSK-3β increased their resistance to various chemotherapeutic drugs and certain small molecule inhibitors. Transfection of cells with KD-GSK-3β often increased therapeutic sensitivity. An exception was observed with cells transfected with WT-GSK-3β and sensitivity to the BCL2/BCLXL ABT737 inhibitor. WT-GSK-3β reduced glycolytic capacity of the cells but did not affect the basal glycolysis and mitochondrial respiration. KD-GSK-3β decreased both basal glycolysis and glycolytic capacity and reduced mitochondrial respiration in MIA-PaCa-2 cells. As a comparison, the effects of GSK-3 on MCF-7 breast cancer cells, which have mutant PIK3CA, were examined. KD-GSK-3β increased the resistance of MCF-7 cells to chemotherapeutic drugs and certain signal transduction inhibitors. Thus, altering the levels of GSK-3β can have dramatic effects on sensitivity to drugs and signal transduction inhibitors which may be influenced by the background of the tumor.

scholarly journals Expression of base excision repair key factors and miR17 in familial and sporadic breast cancer

2014 ◽  
Vol 5 (2) ◽  
pp. e1076-e1076 ◽  
Author(s):  
S De Summa ◽  
R Pinto ◽  
B Pilato ◽  
D Sambiasi ◽  
L Porcelli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Base Excision Repair ◽  
Sporadic Breast Cancer ◽  
Excision Repair ◽  
Key Factors ◽  
Base Excision
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