Evidence of oxidative and nitrosative stress in patients with cervical squamous cell carcinoma

Beevi, Syed Sultan; Rasheed, Muzib Hassanal; Geetha, A

doi:10.1016/j.cca.2006.06.028

Cited by 83 publications

(64 citation statements)

References 27 publications

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“…In prior work, our laboratory explored expression levels of NOS and nitrotyrosine in various carcinomas [9][10][11][12]. Work by other reserachers has demonstrated that NO is overexpressed in multiple cancer types [13][14][15][16][17][18][19]. In vitro studies have alluded to there being NO concentration levels, which when reached, result in phenotypic changes in tumors [20].…”

Section: Introductionmentioning

confidence: 99%

Part I. Molecular and cellular characterization of high nitric oxide-adapted human breast adenocarcinoma cell lines

et al. 2012

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There is a lack of understanding of the casual mechanisms behind the observation that some breast adenocarcinomas have identical morphology and comparatively different cellular growth behavior. This is exemplified by a differential response to radiation, chemotherapy, and other biological intervention therapies. Elevated concentrations of the free radical nitric oxide (NO), coupled with the upregulated enzyme nitric oxide synthase (NOS) which produces NO, are activities which impact tumor growth. Previously, we adapted four human breast cancer cell lines: BT-20, Hs578T, T-47D, and MCF-7 to elevated concentrations of nitric oxide (or high NO [HNO]). This was accomplished by exposing the cell lines to increasing levels of an NO donor over time. Significantly, the HNO cell lines grew faster than did each respective ("PARENT") cell line even in the absence of NO donor-supplemented media. This was evident despite each "parent" being morphologically equivalent to the HNO adapted cell line. Herein, we characterize the HNO cells and their biological attributes against those of the parent cells. Pairs of HNO/parent cell lines were then analyzed using a number of key cellular activity criteria including: cell cycle distribution, DNA ploidy, response to DNA damage, UV radiation response, X-ray radiation response, and the expression of significant cellular enzymes. Other key enzyme activities studied were NOS, p53, and glutathione S-transferase-pi (GST-pi) expression. HNO cells were typified by a far more aggressive pattern of growth and resistance to various treatments than the corresponding parent cells. This was evidenced by a higher S-phase percentage, variable radioresistance, and up-regulated GST-pi and p53. Taken collectively, this data provides evidence that cancer cells subjected to HNO concentrations become resistant to free radicals such as NO via up-regulated cellular defense mechanisms, including p53 and GST-pi. The

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Section: Introductionmentioning

confidence: 99%

Part I. Molecular and cellular characterization of high nitric oxide-adapted human breast adenocarcinoma cell lines

et al. 2012

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“…Its role is strictly dependent upon its chemical reactivity with oxygen and metal. Recent references revealed the involvement of altered NO • level in pathogenesis of CaCx (4). Some of the references showed that NO • in high or low concentration than the basal levels has tumorogenic effect in CaCx (5).…”

Section: Nomentioning

confidence: 99%

Oxidative stress and antioxidant status in cervical cancer patients

Naidu

Suryakar

Swami

et al. 2007

Indian J Clin Biochem

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“…The HPV E6 and E7 oncogenes integrate into the genome of infected cervical cells and inactivate the tumor-suppressor proteins p53 and retinoblastoma, which results in epithelial immortalization and ultimate malignant transformation through a multistage process (1). Due to active and indefinite growth of cancer cells, reactive oxygen species (ROS) production from the mitochondria is accordingly increased (2). Excessive ROS is likely to induce oxidative stress and subsequent cell apoptosis through mitochondria or/ and direct injury to protein, DNA and lipid (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Peroxiredoxin 3 is a novel marker for cell proliferation in cervical cancer

Gao

2012

Biomedical Reports

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Abstract. Although peroxiredoxin 3 (Prx3) has been reported to be involved in cervical cancer (CC) carcinogenesis, the significance of Prx3 in CC progression remains unclear. The present study was conducted to investigate the expression features of Prx3 to better understand the mechanism of tumor growth and invasion. Sixty-eight patients with invasive squamous cervical cancer were included in the present study. The status of human papillomavirus (HPV) infection was detected by hybridization and quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemistry was performed on paraffin-embedded sections using monoclonal antibodies against Prx3 and Ki67. All samples were positive for high-risk HPV, among which fifty-six samples were positive for HPV16, seven for HPV18 and five for HPV33. The expression of HPV16 E6/E7 was significantly higher in cancer areas compared to the adjacent normal epithelial tissuses. The positive cells for Prx3 and Ki67 were significantly higher in cancer cells compared to normal epitheliums and the staining pattern of Prx3 was consistent with that of Ki67 (Pearson's correlation coefficient was 0.801, P= 0.000). The upregulation of Prx3 might be a protective response to oxidative stress in the cancer microenvironment. The expression consistency of Prx3 and Ki67 suggests Prx3 to be a potential marker for cell proliferation of CC.

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Evidence of oxidative and nitrosative stress in patients with cervical squamous cell carcinoma

Cited by 83 publications

References 27 publications

Part I. Molecular and cellular characterization of high nitric oxide-adapted human breast adenocarcinoma cell lines

Part I. Molecular and cellular characterization of high nitric oxide-adapted human breast adenocarcinoma cell lines

Oxidative stress and antioxidant status in cervical cancer patients

Peroxiredoxin 3 is a novel marker for cell proliferation in cervical cancer

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