scholarly journals Xanthohumol, a Prenylated Flavonoid from Hops, Induces DNA Damages in Colorectal Cancer Cells and Sensitizes SW480 Cells to the SN38 Chemotherapeutic Agent

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 932
Author(s):  
Alessandra Scagliarini ◽  
Aline Mathey ◽  
Virginie Aires ◽  
Dominique Delmas
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Anticancer Agents ◽  
Ataxia Telangiectasia Mutated ◽  
Anticancer Compounds ◽  
Dna Damages ◽  
Systematic Screening ◽  
Colorectal Cancer Cells ◽  
Ic50 Values ◽  
First Time

In spite of chemotherapy and systematic screening for people at risk, the mortality rate of colorectal cancer (CRC) remains consistently high, with 600,000 deaths per year. This low success rate in the treatment of CRC results from many failures associated with high resistance and the risk of metastasis. Therefore, in response to these therapeutic failures, new strategies have been under development for several years aimed at increasing the effect of anticancer compounds and/or at reducing their secondary effects on normal cells, thus enabling the host to better withstand chemotherapy. This study highlights that xanthohumol (Xn) concentrations under the IC50 values were able to induce apoptosis and to enhance the DNA-damage response (DDR). We demonstrate for the first time that Xn exerts its anticancer activity in models of colon cancer through activation of the ataxia telangiectasia mutated (ATM) pathway. Subsequently, the ability of Xn to restore DNA damage in CRC cells can sensitize them to anticancer agents such as SN38 (7-ethyl-10-hydroxycamptothecin) used in chemotherapy.

scholarly journals Echinacoside Induces Apoptosis in Human SW480 Colorectal Cancer Cells by Induction of Oxidative DNA Damages

2015 ◽  
Vol 16 (12) ◽  
pp. 14655-14668 ◽  
Author(s):  
Liwei Dong ◽  
Debin Yu ◽  
Nuoting Wu ◽  
Hongge Wang ◽  
Jiajing Niu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Dna Damages ◽  
Colorectal Cancer Cells

scholarly journals Interleukin-6 promotes dietary carcinogen-induced DNA damage in colorectal cancer cells

2015 ◽  
Vol 4 (4) ◽  
pp. 858-866 ◽  
Author(s):  
Saroor A. A. Patel ◽  
Nigel J. Gooderham
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Interleukin 6 ◽  
Inflammatory Cytokine ◽  
Cultured Cells ◽  
Colorectal Cancer Cells ◽  
2D And 3D

Pro-inflammatory cytokine interleukin-6 promotes dietary carcinogen-mediated DNA damage in 2D and 3D cultured cells by inducingCYP1B1expression through miR27b downregulation.

Abstract 3031: Replication stress and DNA damage promote genomic instability in near-tetraploid colorectal cancer cells

2015 ◽  
Author(s):  
Isabel Quintanilla ◽  
Darawalee Wangsa ◽  
Markus Brown ◽  
Amaia Ercilla ◽  
Greg Klus ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Genomic Instability ◽  
Replication Stress ◽  
Colorectal Cancer Cells

scholarly journals Zerumbone increases oxidative stress in a thiol‐dependent ROS ‐independent manner to increase DNA damage and sensitize colorectal cancer cells to radiation

2014 ◽  
Vol 4 (2) ◽  
pp. 278-292 ◽  
Author(s):  
Amit Deorukhkar ◽  
Niharika Ahuja ◽  
Armando‐Lopez Mercado ◽  
Parmeswaran Diagaradjane ◽  
Uma Raju ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Independent Manner ◽  
Colorectal Cancer Cells

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

846: Antitumor activity of the synthetic retinoid ST1926 in colorectal cancer cells: involvement of DNA damage

2014 ◽  
Vol 50 ◽  
pp. S206
Author(s):  
N. Darwiche ◽  
R. Abdel-Samad ◽  
R. Hmadi ◽  
M. El-Sabban ◽  
H. Muhtasib ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Antitumor Activity ◽  
Cancer Cells ◽  
Synthetic Retinoid ◽  
Colorectal Cancer Cells

scholarly journals MicroRNA-18a Attenuates DNA Damage Repair through Suppressing the Expression of Ataxia Telangiectasia Mutated in Colorectal Cancer

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e57036 ◽  
Author(s):  
Chung-Wah Wu ◽  
Yu-Juan Dong ◽  
Qiao-Yi Liang ◽  
Xin-Qi He ◽  
Simon S. M. Ng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Ataxia Telangiectasia ◽  
Dna Damage Repair ◽  
Ataxia Telangiectasia Mutated ◽  
Damage Repair

scholarly journals Ataxia telangiectasia mutated- and Rad3-related kinase drives both the early and the late DNA-damage response to the monofunctional antitumour alkylator S23906

2011 ◽  
Vol 437 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Daniele G. Soares ◽  
Aude Battistella ◽  
Céline J. Rocca ◽  
Renata Matuo ◽  
João A. P. Henriques ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Anticancer Agents ◽  
Ataxia Telangiectasia ◽  
Kinase Inhibitors ◽  
Protein A ◽  
Initial Response ◽  
Synergistic Activity ◽  
Ataxia Telangiectasia Mutated ◽  
Damage Response

Numerous anticancer agents and environmental mutagens target DNA. Although all such compounds interfere with the progression of the replication fork and inhibit DNA synthesis, there are marked differences in the DNA-damage response pathways they trigger, and the relative impact of the proximal or the distal signal transducers on cell survival is mainly lesion-specific. Accordingly, checkpoint kinase inhibitors in current clinical development show synergistic activity with some DNA-targeting agents, but not with others. In the present study, we characterize the DNA-damage response to the antitumour acronycine derivative S23906, which forms monofunctional adducts with guanine residues in the minor groove of DNA. S23906 exposure is accompanied by specific recruitment of RPA (replication protein A) at replication sites and rapid Chk1 activation. In contrast, neither MRN (Mre11-Rad50-Nbs1) nor ATM (ataxia-telangiectasia mutated), contributes to the initial response to S23906. Interestingly, genetic attenuation of ATR (ATM- and Ras3-related) activity inhibits not only the early phosphorylation of histone H2AX and Chk1, but also interferes with the late phosphorylation of Chk2. Moreover, loss of ATR function or pharmacological inhibition of the checkpoint kinases by AZD7762 is accompanied by abrogation of the S-phase arrest and increased sensitivity towards S23906. These findings identify ATR as a central co-ordinator of the DNA-damage response to S23906, and provide a mechanistic rationale for combinations of S23906 and similar agents with checkpoint abrogators.

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