scholarly journals Loss of ID3 in pancreatic cancer cells increases DNA damage without impairing MDC1 recruitment to the nuclear foci

2021 ◽  
Author(s):  
Jian Xu ◽  
Mayrel Palestino Dominguez ◽  
Christine Alewine
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Pancreatic Cancer Cells ◽  
Nuclear Foci

scholarly journals APE2 Is a General Regulator of the ATR-Chk1 DNA Damage Response Pathway to Maintain Genome Integrity in Pancreatic Cancer Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Md Akram Hossain ◽  
Yunfeng Lin ◽  
Garrett Driscoll ◽  
Jia Li ◽  
Anne McMahon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Human Pancreatic Cancer ◽  
Genome Integrity ◽  
Pancreatic Cancer Cells ◽  
Damage Response ◽  
Egg Extracts

The maintenance of genome integrity and fidelity is vital for the proper function and survival of all organisms. Recent studies have revealed that APE2 is required to activate an ATR-Chk1 DNA damage response (DDR) pathway in response to oxidative stress and a defined DNA single-strand break (SSB) in Xenopus laevis egg extracts. However, it remains unclear whether APE2 is a general regulator of the DDR pathway in mammalian cells. Here, we provide evidence using human pancreatic cancer cells that APE2 is essential for ATR DDR pathway activation in response to different stressful conditions including oxidative stress, DNA replication stress, and DNA double-strand breaks. Fluorescence microscopy analysis shows that APE2-knockdown (KD) leads to enhanced γH2AX foci and increased micronuclei formation. In addition, we identified a small molecule compound Celastrol as an APE2 inhibitor that specifically compromises the binding of APE2 but not RPA to ssDNA and 3′-5′ exonuclease activity of APE2 but not APE1. The impairment of ATR-Chk1 DDR pathway by Celastrol in Xenopus egg extracts and human pancreatic cancer cells highlights the physiological significance of Celastrol in the regulation of APE2 functionalities in genome integrity. Notably, cell viability assays demonstrate that APE2-KD or Celastrol sensitizes pancreatic cancer cells to chemotherapy drugs. Overall, we propose APE2 as a general regulator for the DDR pathway in genome integrity maintenance.

scholarly journals Pharmacologic Ascorbate Primes Pancreatic Cancer Cells for Death by Rewiring Cellular Energetics and Inducing DNA Damage

2019 ◽  
Vol 17 (10) ◽  
pp. 2102-2114 ◽  
Author(s):  
Visarut Buranasudja ◽  
Claire M. Doskey ◽  
Adrienne R. Gibson ◽  
Brett A. Wagner ◽  
Juan Du ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Pancreatic Cancer Cells ◽  
Cellular Energetics

Radiosensitization of metformin in pancreatic cancer cells via abrogating the G2 checkpoint and inhibiting DNA damage repair

2015 ◽  
Vol 369 (1) ◽  
pp. 192-201 ◽  
Author(s):  
Zheng Wang ◽  
Song-Tao Lai ◽  
Ning-Yi Ma ◽  
Yun Deng ◽  
Yong Liu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Repair ◽  
G2 Checkpoint ◽  
Pancreatic Cancer Cells ◽  
Damage Repair

scholarly journals A preliminary study on the synthetic lethal effect of berberine and olaparib on pancreatic cancer cells and its mechanism

2021 ◽  
Vol 233 ◽  
pp. 02023
Author(s):  
Chengyong Zhang ◽  
Tingting Yang ◽  
Xiaoting Chen ◽  
Jiexuan Xu ◽  
Danlu Liang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Oxidative Dna Damage ◽  
Parp Inhibitor ◽  
Cell Activity ◽  
Lethal Effect ◽  
Synthetic Lethal ◽  
Pancreatic Cancer Cells ◽  
Apoptosis Inhibitor

Pancreatic cancer is a kind of malignant tumor with high mortality rate. Early operation and late chemoradiotherapy are the treatment criteria, but the prognosis is still poor. Berberine, an alkaloid compound present in many herbal plants, is capable of inducing oxidative DNA damage and downregulating homologous recombination repair (HRR) in cancer cells. Poly (ADP ribose) polymerase-1 (PARP-1) is a sensor of DNA damage with key roles in DNA repair. In this study, we demonstrated that berberine and PARP inhibitor olaparib have a synthetic lethal effect on pancreatic cancer cells. The expression level of RAD51 were reduced by berberine. Correspondingly, PARP became hyperactivated in response to berberine treatment. When berberine is combined with olaparib, the expression of Rad51 and Parp are inhibited. The combination of berberine and olaparib synergistically inhibit cell activity and induce cell apoptosis. In addition, the synergistic effect of berberine and olaparib can be reversed by apoptosis inhibitor and necrosis inhibitor. Together, the results indicate that berberine combined with olaparib have a synthetic lethal effect on pancreatic cancer cells.

Abstract A18: HuR, an RNA binding protein, is critical for the DNA damage response in pancreatic cancer cells.

2012 ◽  
Author(s):  
Shruti Lal ◽  
Vikram Bhattacharjee ◽  
Timothy Yen ◽  
Richard A. Burkhart ◽  
Danielle M. Pineda ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Pancreatic Cancer Cells ◽  
Damage Response

Ascorbate Augments Radiation-induced DNA Damage and Cytotoxicity in Pancreatic Cancer Cells

2010 ◽  
Vol 49 ◽  
pp. S58-S59
Author(s):  
Juan Du ◽  
Amanda Kalen ◽  
Zita Sibenaller ◽  
Prabhat Goswami ◽  
Joseph Cullen
Keyword(s):  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Pancreatic Cancer Cells ◽  
Radiation Induced

scholarly journals Sulforaphane enhances irradiation effects in terms of perturbed cell cycle progression and increased DNA damage in pancreatic cancer cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (7) ◽  
pp. e0180940 ◽  
Author(s):  
Patrick Naumann ◽  
Jakob Liermann ◽  
Franco Fortunato ◽  
Thomas E. Schmid ◽  
Klaus-Josef Weber ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Irradiation Effects ◽  
Cycle Progression ◽  
Pancreatic Cancer Cells
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