scholarly journals The mismatch repair protein hMLH1 regulates selenium‐induced DNA damage response in colorectal cancer cells

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Yongmei Qi ◽  
Norberta W Schoene ◽  
Wen‐Hsing Cheng
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Repair Protein ◽  
Colorectal Cancer Cells ◽  
Damage Response ◽  
Mismatch Repair Protein

scholarly journals Correction: Down-regulation of G9a triggers DNA damage response and inhibits colorectal cancer cells proliferation

Oncotarget ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 302-303
Author(s):  
Jie Zhang ◽  
Pengxing He ◽  
Yong Xi ◽  
Meiyu Geng ◽  
Yi Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Down Regulation ◽  
Colorectal Cancer Cells ◽  
Damage Response

scholarly journals Down-regulation of G9a triggers DNA damage response and inhibits colorectal cancer cells proliferation

Oncotarget ◽  
2015 ◽  
Vol 6 (5) ◽  
pp. 2917-2927 ◽  
Author(s):  
Jie Zhang ◽  
Pengxing He ◽  
Yong Xi ◽  
Meiyu Geng ◽  
Yi Chen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Down Regulation ◽  
Colorectal Cancer Cells ◽  
Damage Response

KDM4B promotes DNA damage response via STAT3 signaling and is a target of CREB in colorectal cancer cells

2018 ◽  
Vol 449 (1-2) ◽  
pp. 81-90 ◽  
Author(s):  
Wei-Wu Deng ◽  
Qian Hu ◽  
Zheng-Ren Liu ◽  
Qiu-Hong Chen ◽  
Wen-Xiang Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Stat3 Signaling ◽  
Colorectal Cancer Cells ◽  
Damage Response

scholarly journals DNMT1 deficiency triggers mismatch repair defects in human cells through depletion of repair protein levels in a process involving the DNA damage response

2011 ◽  
Vol 20 (16) ◽  
pp. 3241-3255 ◽  
Author(s):  
Jayne E.P. Loughery ◽  
Philip D. Dunne ◽  
Karla M. O'Neill ◽  
Richard R. Meehan ◽  
Jennifer R. McDaid ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Human Cells ◽  
Protein Levels ◽  
Repair Protein ◽  
Damage Response

scholarly journals Olaparib-mediated enhancement of 5-fluorouracil cytotoxicity in mismatch repair deficient colorectal cancer cells

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Helena de Castro e Gloria ◽  
Laura Jesuíno Nogueira ◽  
Patrícia Bencke Grudzinski ◽  
Paola Victória da Costa Ghignatti ◽  
Temenouga Nikolova Guecheva ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Mismatch Repair ◽  
Cell Cycle Progression ◽  
Combined Therapy ◽  
Combined Treatment ◽  
Human Colon ◽  
Human Colon Cancer

Abstract Background The advances in colorectal cancer (CRC) treatment include the identification of deficiencies in Mismatch Repair (MMR) pathway to predict the benefit of adjuvant 5-fluorouracil (5-FU) and oxaliplatin for stage II CRC and immunotherapy. Defective MMR contributes to chemoresistance in CRC. A growing body of evidence supports the role of Poly-(ADP-ribose) polymerase (PARP) inhibitors, such as Olaparib, in the treatment of different subsets of cancer beyond the tumors with homologous recombination deficiencies. In this work we evaluated the effect of Olaparib on 5-FU cytotoxicity in MMR-deficient and proficient CRC cells and the mechanisms involved. Methods Human colon cancer cell lines, proficient (HT29) and deficient (HCT116) in MMR, were treated with 5-FU and Olaparib. Cytotoxicity was assessed by MTT and clonogenic assays, apoptosis induction and cell cycle progression by flow cytometry, DNA damage by comet assay. Adhesion and transwell migration assays were also performed. Results Our results showed enhancement of the 5-FU citotoxicity by Olaparib in MMR-deficient HCT116 colon cancer cells. Moreover, the combined treatment with Olaparib and 5-FU induced G2/M arrest, apoptosis and polyploidy in these cells. In MMR proficient HT29 cells, the Olaparib alone reduced clonogenic survival, induced DNA damage accumulation and decreased the adhesion and migration capacities. Conclusion Our results suggest benefits of Olaparib inclusion in CRC treatment, as combination with 5-FU for MMR deficient CRC and as monotherapy for MMR proficient CRC. Thus, combined therapy with Olaparib could be a strategy to overcome 5-FU chemotherapeutic resistance in MMR-deficient CRC.

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