Alteration of pRb expression in the development of rat tongue carcinoma induced by 4-nitroquinoline 1-oxide

Niwa, Shinya; Ueno, Shinji; Shirasu, Rikiya

doi:10.1016/s1368-8375(00)00141-x

Cited by 30 publications

(25 citation statements)

References 16 publications

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“…Methylation analysis in oral cancer also revealed variation in the frequency of methylation of genes depending on the intra-oral sites (Ogi et al 2002). Experimental oral carcinogenic studies reported site-speciWc diVerence in the biology of oral carcinogenesis (Schwartz et al 2000;Niwa et al 2001). Along with these studies, our results indicate that oral carcinoma of diVerent anatomical subsites is characterized by alterations at diVerent pathways.…”

Section: Discussionsupporting

confidence: 75%

Carcinoma of tongue and the buccal mucosa represent different biological subentities of the oral carcinoma

Sathyan

Sailasree

Jayasurya

et al. 2006

J Cancer Res Clin Oncol

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Section: Discussionsupporting

confidence: 75%

Carcinoma of tongue and the buccal mucosa represent different biological subentities of the oral carcinoma

Sathyan

Sailasree

Jayasurya

et al. 2006

J Cancer Res Clin Oncol

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“…41,42) Cyclin D1 overexpression has been reported in human cancers of the head and neck, including tongue, and in 4-NQO-induced tongue cancers of rats, which leads to dysregulation of cell cycle and uncontrolled cell proliferation. [43][44][45] Hence, the decreased cyclin D1 expression in the present study may play an important role in the suppression of tongue carcinogenesis by troglitazone.…”

Section: Discussionmentioning

confidence: 72%

Inhibitory effects of troglitazone, a peroxisome proliferator‐activated receptor γ ligand, in rat tongue carcinogenesis initiated with 4‐nitroquinoline 1‐oxide

Yoshida

Hirose²,

Tanaka

et al. 2003

Cancer Science

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Ligands for peroxisome proliferator-activated receptor (PPAR) γ γ γ γ have been implicated in growth inhibition and cell differentiation in certain malignancies. In this study, the effects of troglitazone, a PPARγ γ γ γ ligand, given during the postinitiation phase of oral carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. Rats aged 6 weeks were given 4-NQO at 20 ppm for 8 weeks to induce tongue neoplasms. Starting 1 week after the cessation of 4-NQO exposure, animals were fed diets containing 0, 30 or 100 ppm troglitazone for 22 weeks. At the end of the study (week 32), the incidences of 4-NQO-induced tongue neoplasms and preneoplasms were determined histopathologically and cell proliferation activity was estimated by counting bromodeoxyuridine (BrdU)-labeling indices and cyclin D1-positive cell ratios. In addition, immunohistochemical expression of cyclooxygenase (COX)-2 and PPARγ γ γ γ was assessed in the tongue lesions. Feeding with 100 ppm troglitazone significantly decreased the incidence of squamous cell carcinoma when compared to the group without troglitazone treatment (5.0% vs. 45.8%, P < < < <0.005). Interestingly, the BrdU-labeling index and cyclin D1-positive cell ratio assessed in the non-lesional tongue squamous epithelium were reduced by dietary administration of troglitazone (P < < < <0.0001-0.005). Additionally, the immunoreactivity of COX-2 in the tongue lesions was also decreased by the treatment (P < < < <0.01-0.05). These results clearly showed that dietary troglitazone inhibits 4-NQO-induced tongue carcinogenesis and such inhibition is related to suppression of increased cell proliferation and/or COX-2 expression. This study warrants further investigation on the use of PPARγ γ γ γ ligands as a novel preventive approach for oral malignancy. (Cancer Sci 2003; 94: 365-371) he nuclear receptor superfamily acts as ligand-responsive transcription factors that participate in many processes important for cell and tissue homeostasis. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor superfamily that includes receptors for steroids, thyroid hormone, vitamin D or retinoic acid.1) At present, several PPARs including PPARα, PPARβ (PPARδ, NUC-1, or FAAR), and PPARγ have been identified.2) Of these, PPARγ was initially shown to have regulatory roles in insulin sensitization. 3,4) The receptor binds to the promoter region of target genes involved in adipocyte differentiation and lipid storage [4][5][6] as a heterodimer with the retinoid X receptor.7) Activation of this receptor has been implicated in glucose metabolism, cell cycle control, and macrophage development and function. [8][9][10][11][12] In addition, recent studies suggest that PPARs play an important role in carcinogenesis. 13) 15-Deoxy-δ-prostaglandin J 2 , a natural-occurring metabolite of prostaglandin D 2 , and troglitazone, a thiazolidinedione analogue and a synthetic anti-diabetic drug, have been reported to be selective ligands for PPARγ.9, 14, 15) Re...

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“…The immunohistochemical technique that we have used in this in vivo test-system overcomes these problems. Indeed, this technique has widely been applied to study apoptosis and carcinogenesis in oral tissues from rodents (Niwa et al 2001;Nishimura 1999;Okazaki et al 2002). In normal tongue epithelia, represented by the negative control group, bcl-2 protein was restrictedly present in basal and supra-basal layers.…”

Section: Discussionmentioning

confidence: 99%

Cigarette Smoke Affects Apoptosis in Rat Tongue Mucosa: Role of bcl-2 Gene Family

Assis¹,

Ceolin²,

Marques

et al. 2006

J Mol Hist

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While it has been clearly demonstrated that smoking is the most significant exogenous factor involved in oral carcinogenesis, little is known about the global molecular and cellular changes that occur prior to the appearance of clinically detectable symptoms. Thus, the aim of this study was to investigate the expressivity of bcl-2, bax and PCNA in the rat tongue mucosa exposed to cigarette smoke by means of immunohistochemistry. A total of twelve male Wistar rats were distributed into 2 groups: negative control and experimental group exposed to cigarette smoke during 75 days. After experimental period, no histopathological changes in the tongue mucosa were detected in the negative control and the experimental group. On the other hand, an overexpression of bcl-2 was detected (p < 0.01) throughout all layers of the epithelium, whereas bax did not show significant differences (p > 0.05). Also, the labeling index for bcl-2 and bax showed an increase 75 days after cigarette exposure (p < 0.01). PCNA-labeling index did not show remarkable changes between groups. Taken together, our results show that bcl-2 is overexpressed in the rat tongue keratinocytes after cigarette smoke exposure.

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Alteration of pRb expression in the development of rat tongue carcinoma induced by 4-nitroquinoline 1-oxide

Cited by 30 publications

References 16 publications

Carcinoma of tongue and the buccal mucosa represent different biological subentities of the oral carcinoma

Carcinoma of tongue and the buccal mucosa represent different biological subentities of the oral carcinoma

Inhibitory effects of troglitazone, a peroxisome proliferator‐activated receptor γ ligand, in rat tongue carcinogenesis initiated with 4‐nitroquinoline 1‐oxide

Cigarette Smoke Affects Apoptosis in Rat Tongue Mucosa: Role of bcl-2 Gene Family

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