Up-regulation of glutathione-related genes, enzyme activities and transport proteins in human cervical cancer cells treated with doxorubicin

Drozd, Ewa; Krzysztoń-Russjan, Jolanta; Marczewska, J; Drozd, Janina; Bubko, Irena; Bielak, Magda; Lubelska, Katarzyna; Wiktorska, Katarzyna; Chilmończyk, Zdzisław; Anuszewska, Elżbieta; Gruber-Bzura, Beata M

doi:10.1016/j.biopha.2016.06.051

Cited by 25 publications

(17 citation statements)

References 39 publications

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“…76 They also suggested that the upregulation of GSTM1 and GSTA1-3 is correlated with drug resistance of cells. 76 Similarly, Filippova et al found that drug-sensitive CC cells have lower levels of antioxidant enzymes compared with resistant cells. 77 Reduced expression of antioxidant enzymes results in increased levels of ROS and subsequent ROS-mediated tumor cell death.…”

Section: Oxidative Stress and Chemo/radiotherapy Resistancementioning

confidence: 99%

Oxidative stress in cervical cancer pathogenesis and resistance to therapy

Ebrahimi

Soltani

Hashemy

2018

J of Cellular Biochemistry

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Cervical cancer (CC) is one of the most common cancers among females, and it is most notable in developing countries. The exact etiology of CC is poorly understood; but, smoking, oral contraceptives, immunosuppression, and infection with human papillomavirus (HPV) may increase the risk of CC. There is also an association between CC and oxidative stress. Oxidative stress is caused by a disturbed oxidant‐antioxidant balance in favor of the former, leading to an excessive generation of free radicals, particularly reactive oxygen species (ROS), and subsequently to biological damages. Thus, redox enzymatic and nonenzymatic regulators are required to maintain the redox homeostasis. Dysregulated antioxidants system and the pathogenic role of oxidative stress in CC have been investigated in several clinical and preclinical studies. In this study, we reviewed studies that have addressed the cross‐talk between oxidative stress and CC pathogenesis and resistance to therapy.

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Section: Oxidative Stress and Chemo/radiotherapy Resistancementioning

confidence: 99%

Oxidative stress in cervical cancer pathogenesis and resistance to therapy

Ebrahimi

Soltani

Hashemy

2018

J of Cellular Biochemistry

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“…GSH pathway is involved in cell detoxification and antioxidation and may be associated with oncogenesis, prognosis, and response to treatment [18, 19]. Therefore, genetic variants in the GSH pathway would influence cancer recurrence and response to BCG treatment after TURBT in NMIBC patients.…”

Section: Evidence Synthesismentioning

confidence: 99%

Prediction of Bacillus Calmette-Guerin Response in Patients with Bladder Cancer after Transurethral Resection of Bladder Tumor by Using Genetic Variation Based on Genomic Studies

Zhang

Jiang

Liu

et al. 2016

BioMed Research International

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Purpose. We aimed to comprehensively review contemporary literature on genetic and epigenetic biomarkers associated with the prediction of Bacillus Calmette-Guerin (BCG) response after the transurethral resection of a bladder tumor and to discuss the application of these biomarkers in precision cancer care for bladder cancer. Method. We performed a systematic review of published literatures in the databases PubMed and Embase by using the following key words: bladder cancer, BCG, gene, and methylation. Studies associated with cell lines, animal models, and muscle invasive bladder cancer were excluded. Results. The genetic variations associated with BCG response can be classified into three categories: germline variations, somatic variations, and epigenetic alterations. Genes related to BCG response were mainly involved in single-nucleotide polymorphisms, copy number variations, and gene methylations. Conclusions. Although these gene alterations are currently the most promising predictive markers of BCG response, most studies about bladder cancer DNA biomarkers are related to germline variations in candidate genes, and the results are not consistent. Only one study is related to somatic variation, and further evaluation in large-scale validation studies should be conducted to assess the potential clinical application of these findings. In addition, other biomarkers based on different “–omics” technologies should be considered in future studies.

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“…Additionally, GSH‐based detoxification also causes apoptosis resistance in numerous cancer cells . Thus, excessive ROS production along with GSH depletion can effectively enhance anti‐cancer drug activity and overcome drug resistance …”

Section: Introductionmentioning

confidence: 99%

“…[15][16][17] Thus, excessive ROS production along with GSH depletion can effectively enhance anti-cancer drug activity and overcome drug resistance. [18][19][20] Apoptosis has been a prevalent model in anti-cancer drug development, but de-regulated apoptotic signalling often leads to an increase of apoptosis resistance in cancer cells with the progression of treatment. 21,22 Additionally, autophagy has been proposed as a tumour suppressor, plays a key pro-survival role in cells by eliminating damaged organelles and proteins, and contributes apoptosis resistance in cancer cells.…”

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confidence: 99%