Nitric oxide synthase activity in human squamous cell carcinoma of the head and neck

Gavilanes, Javier; Moro, Marı́a A.; Lizasoaín, Ignacio; Lorenzo, Pedro; Pérez, Ana; Leza, Juan C.; Álvarez-Vicent, Juan José

doi:10.1097/00005537-199901000-00028

Cited by 29 publications

(34 citation statements)

References 18 publications

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“…6 In this respect the high NOS2 expression of severe dysplasia noted in our study suggests that this process begins to occur before the transformation into invasive cancer.…”

Section: Discussionmentioning

confidence: 52%

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Does type II nitric oxide synthase expression correlate with cellular proliferation in oral squamous cell carcinoma and dysplasia?

et al. 2001

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“…6 In this respect the high NOS2 expression of severe dysplasia noted in our study suggests that this process begins to occur before the transformation into invasive cancer.…”

Section: Discussionmentioning

confidence: 52%

“…[5][6][7] These studies demonstrated significantly increased expression and activity of NOS2 in tumor tissue. Enhanced angiogenesis also correlated with NO production both in resected tumor specimens and in an animal model, the rabbit cornea.…”

mentioning

confidence: 82%

Does type II nitric oxide synthase expression correlate with cellular proliferation in oral squamous cell carcinoma and dysplasia?

et al. 2001

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“…As indicated in our prior works, a number of tumor cell lines have been adapted to HNO concentration levels including those from lung [11,[46][47][48], head and neck [3,[49][50][51][52], and breast [7], suggesting that NO adaptation is also a universal property. In an attempt to further elucidate the impact of extended exposure from NO on underlying biological systems, we herein characterize the four newly The ten most up-regulated appear first and the ten most down-regulated appear below within each cell line type NA not available a Gene symbols used vary according to the supplier of the gene chip created breast adenocarcinoma HNO cell lines [7], along with each respective parent cell line.…”

Section: Resultsmentioning

confidence: 85%

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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“…NO is termed as a ‘double-edged sword’ as it possesses both beneficial and deleterious effects depending on the amounts and conditions under which it is produced [54]. However, high NO production is required in the early stage of head and neck carcinoma, leading to iNOS expression in order to activate angiogenesis [55]and enhance tumor cell adhesivity and permeability [56]. Thus, a new cancer therapy by preventing angiogenesis, invasion, and metastasis through inhibition of NOS generation is proposed [34]and experimental drugs for specific iNOS inhibitors, such as 1400W [57], have been developed.…”

Section: Discussionmentioning

confidence: 99%

A Novel Geranylated Derivative, Ethyl 3-(4′-Geranyloxy-3′-Methoxyphenyl)-2-Propenoate, Synthesized from Ferulic Acid Suppresses Carcinogenesis and Inducible Nitric Oxide Synthase in Rat Tongue

Tanaka¹,

Kohno

Nomura

et al. 2003

Oncology

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Objectives: We have previously observed the inhibitory effect of ferulic acid on rat tongue carcinogenesis. In this study, we investigated the modifying effects of a novel geranylated derivative, ethyl 3-(4′-geranyloxy-3′-methoxyphenyl)-2-propenoate (EGMP), synthesized from ferulic acid on tongue carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO). Methods: F344 male rats except those treated with EGMP alone and untreated rats were given 20 ppm 4-NQO in drinking water for 9 weeks to induce tongue neoplasms. Starting 1 week after the cessation of exposure to 4-NQO, the experimental groups given 4-NQO and a basal diet were fed the experimental diets containing EGMP (0.2% and 2%) for 20 weeks. The activities of glutathione S-transferase (GST) and quinone reductase (QR), the expression of proliferating cell nuclear antigen, polyamine content and ornithine decarboxylase activity in the tongue were examined for mechanistic analysis of modifying effects of EGMP on carcinogenesis. The expression of inducible nitric acid synthase (iNOS) was also assessed immunohistochemically. Results: At week 30, the incidence and multiplicity of tongue squamous cell carcinoma were significantly reduced by feeding of a 2% EGMP diet. EGMP feeding (2% in diet) elevated tongue GST activity and lowered QR activity in the tongue. Dietary EGMP decreased the expression of cell proliferation biomarker expression. Interestingly, EGMP feeding altered iNOS expression in the invasive parts of carcinoma. Conclusions: These results suggest that EGMP, when given at the 2% dose level during the promotion phase, exerts a chemopreventive action against tongue tumorigenesis through modification of cell proliferation activity and/or detoxifying enzymatic activity.

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Nitric oxide synthase activity in human squamous cell carcinoma of the head and neck

Cited by 29 publications

References 18 publications

Does type II nitric oxide synthase expression correlate with cellular proliferation in oral squamous cell carcinoma and dysplasia?

Does type II nitric oxide synthase expression correlate with cellular proliferation in oral squamous cell carcinoma and dysplasia?

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

A Novel Geranylated Derivative, Ethyl 3-(4′-Geranyloxy-3′-Methoxyphenyl)-2-Propenoate, Synthesized from Ferulic Acid Suppresses Carcinogenesis and Inducible Nitric Oxide Synthase in Rat Tongue

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