The Role of Oxidative Stress in the Development of Cisplatin Resistance in Epithelial Ovarian Cancer

Belotte, J; Fletcher, N.M.; Awonuga, Awoniyi O.; Alexis, Mitchell; Abu-Soûd, Husam M.; Saed, Mohammed G.; Diamond, Michael P.; Saed, Ghassan M.

doi:10.1177/1933719113503403

Cited by 33 publications

(28 citation statements)

References 36 publications

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“…Pro-oxidant enzymes such as myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS) and NAD(P)H oxidase have been associated with initiation, progression, survival, and increased risk in cancers such as breast, ovarian, lung, prostate, bladder, colorectal and malignant melanoma [21,44]. Moreover, the expression of those key pro-oxidant enzymes was found to change based on the histological type and grade of the tumor [21,45,46]. Likewise, antioxidants have also been associated with initiation, progression, survival, and increased risk in cancers such as lung, head and neck, and prostate cancer [47][48][49][50].…”

Section: Cancer Cells Are Under Intrinsic Oxidative Stressmentioning

confidence: 99%

“…The expression of GSR and GPX, key antioxidant enzymes, has also been reported to be altered in various types of cancer [21]. The activity and expression of SOD, a powerful antioxidant enzyme, has been reported to be decreased in colorectal carcinomas, pancreatic, lung, gastric, ovarian, and breast cancers [21,45,46]. Likewise, the expression and activity of CAT, a key antioxidant enzyme, was reported to be decreased in breast, bladder, and lung cancers but increased in brain cancer [21,45,46].…”

Section: Cancer Cells Are Under Intrinsic Oxidative Stressmentioning

confidence: 99%

“…The activity and expression of SOD, a powerful antioxidant enzyme, has been reported to be decreased in colorectal carcinomas, pancreatic, lung, gastric, ovarian, and breast cancers [21,45,46]. Likewise, the expression and activity of CAT, a key antioxidant enzyme, was reported to be decreased in breast, bladder, and lung cancers but increased in brain cancer [21,45,46]. Antioxidant enzymes play a critical role in maintaining the redox balance in the presence of microenvironment stress, and thus, alteration of this balance may provide a unique and complex microenvironment for cancer cell survival.…”

Section: Cancer Cells Are Under Intrinsic Oxidative Stressmentioning

confidence: 99%

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New Insights into the Pathogenesis of Ovarian Cancer: Oxidative Stress

Saed¹,

Morris²,

Fletcher³

2018

Ovarian Cancer - From Pathogenesis to Treatment

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Ovarian cancer is the leading cause of death from gynecologic malignancies yet the underlying pathophysiology is not clearly established. Epithelial ovarian cancer (EOC) has long been considered a heterogeneous disease with respect to histopathology, molecular biology, and clinical outcome. Treatment of ovarian cancer includes a combination of cytoreductive surgery and combination chemotherapy, with platinums and taxanes. Despite initial success, over 75% of patients with advanced disease will relapse around 18 months and the overall 5-year survival is approximately 50%. Cancer cells are known to be under intrinsic oxidative stress, which alters their metabolic activity and reduces apoptosis. Epithelial ovarian cancer has been shown to manifest a persistent pro-oxidant state as evident by the upregulation of several key oxidant enzymes in EOC tissues and cells. In the light of our scientific research and the most recent experimental and clinical observations, this chapter provides the reader with up to date most relevant findings on the role of oxidative stress in the pathogenesis and prognosis of ovarian cancer, as well as a novel mechanism of apoptosis/survival in EOC cells.

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Section: Cancer Cells Are Under Intrinsic Oxidative Stressmentioning

confidence: 99%

Section: Cancer Cells Are Under Intrinsic Oxidative Stressmentioning

confidence: 99%

Section: Cancer Cells Are Under Intrinsic Oxidative Stressmentioning

confidence: 99%

See 1 more Smart Citation

New Insights into the Pathogenesis of Ovarian Cancer: Oxidative Stress

Saed¹,

Morris²,

Fletcher³

2018

Ovarian Cancer - From Pathogenesis to Treatment

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“…Furthermore, the functional role of TRAIL and the mechanisms of TRAIL tolerance require elucidation. Recently, cisplatin has been proven to produce oxidative stress in vivo and in vitro (8)(9)(10). Some research groups have demonstrated that different levels of oxidative stress can determine cancer cell fate (11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Mild oxidative stress induced by a low dose of cisplatin contributes to the escape of TRAIL-mediated apoptosis in the ovarian cancer SKOV3 cell line

Zhang

Xie

et al. 2016

Oncology Reports

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Tumor necrosis factor (TNF)-related apoptosis‑inducing ligand (TRAIL) is expressed in ovarian tissue and is widely thought to exhibit strong antitumor activity in a variety of tumor cell types. Therefore, we hypothesized that the cisplatin resistance of ovarian cancer is linked to the ability to escape from TRAIL-mediated apoptosis. We demonstrated that cisplatin-resistant ovarian cancer cell line SKOV3/DDP tolerated treatment with TRAIL, in contrast to the cisplatin‑sensitive ovarian cancer cell line SKOV3. SKOV3/DDP cells exhibited a much higher cell viability and a lower apoptosis rate than SKOV3 cells after treatment with TRAIL. To determine whether cisplatin induced the tolerance of TRAIL, we pretreated the SKOV3 cells with cisplatin in the presence of TRAIL. This revealed that a low dose of cisplatin (1 µM) increased the TRAIL tolerance of SKOV3 cells. Furthermore, cisplatin induced oxidative stress in both the SKOV3/DDP and SKOV3 cells, although the oxidative stress level of the SKOV3/DDP cells was generally much higher than that noted in the SKOV3 cells. Similarly, a low dose of hydrogen peroxide increased the TRAIL tolerance in SKOV3 cells. Notably, the TRAIL tolerance in the SKOV3 and SKOV3/DDP cells could be abrogated by the oxidative stress scavenger N-acetyl-cysteine. These results suggest that a low dose of cisplatin induces the tolerance of TRAIL in SKOV3 cells at least partly, depending on the oxidative stress signaling pathway.

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“…Cisplatin is a commonly used chemotherapeutic agent that exerts a therapeutic effect in various types of cancer and is often used to treat female patients at a reproductive age; however, despite its therapeutic effect, the side effects of cisplatin have also received considerable attention. The side effects of cisplatin are associated with an excessive production of free radicals and ROS, such as superoxide anions or H 2 O 2 , in different kidney cells (19) and in ovarian cancer (6,20). To investigate the side effects of cisplatin on the ovaries in the present study, an intraperitoneal injection of cisplatin was used to induce ovarian injury in female rats of a reproductive age.…”

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confidence: 99%

Hydrogen-rich saline attenuates chemotherapy-induced ovarian injury via regulation of oxidative stress

Meng

Chen

Wang

et al. 2015

Experimental and Therapeutic Medicine

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Hydrogen has been reported to exert a therapeutic effect in several diseases due to its antioxidative, anti-inflammatory and anti-apoptotic properties. The aim of the present study was to investigate whether hydrogen-rich saline treatment could attenuate ovarian damage induced by cisplatin. A total of 240 adult, virgin, female Sprague Dawley rats, weighing 180-220 g, were randomly divided into four groups (n=60 per group): Control (Con), control + hydrogen-rich saline (Con + H), cisplatin-induced ovarian injury (OI) and cisplatin-induced ovarian injury + hydrogen-rich saline (OI + H). Cisplatin was diluted in saline immediately before use. In the OI and OI + H groups, the rats were administered a dose of cisplatin on the 1st and 7th days. The rats in the Con + H and OI + H groups were intraperitoneally injected with hydrogen-rich saline (10ml/kg body weight) once a day over a 2-week period. On the 14th, 28th and 42nd days (T, T and T) after the cisplatin injection, femoral vein blood was collected. At the end of the experiment, ovarian homogenates were prepared, and the samples were used for estrogen (E), follicle-stimulating hormone (FSH), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) examination. In addition, rats (n=10 per group) were sacrificed for bilateral ovary removal; one was fixed in formalin for follicle-counting analysis, while the other was used for nuclear factor erythroid 2-related factor 2 (Nrf2) detection by western blotting. Hydrogen-rich saline attenuated the FSH release, elevated the level of E, improved the development of follicles, and reduced the damage to the ovarian cortex at T, T and T in the OI + H rats. Cisplatin induced oxidative stress by increasing the levels of oxidation products and attenuating the activity of antioxidant enzyme, which could be reversed by hydrogen-rich saline treatment. Furthermore, hydrogen-rich saline regulated the Nrf2 protein expression in rats with ovarian damage. In conclusion, hydrogen-rich saline exerts a protective effect against cisplatin-induced ovarian injury by reducing MDA and increasing SOD and CAT activity. Ovarian injury induced by chemotherapy involves the activation of Nrf2.

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The Role of Oxidative Stress in the Development of Cisplatin Resistance in Epithelial Ovarian Cancer

Cited by 33 publications

References 36 publications

New Insights into the Pathogenesis of Ovarian Cancer: Oxidative Stress

New Insights into the Pathogenesis of Ovarian Cancer: Oxidative Stress

Mild oxidative stress induced by a low dose of cisplatin contributes to the escape of TRAIL-mediated apoptosis in the ovarian cancer SKOV3 cell line

Hydrogen-rich saline attenuates chemotherapy-induced ovarian injury via regulation of oxidative stress

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