Apigenin prevents deregulation in the expression pattern of cell-proliferative, apoptotic, inflammatory and angiogenic markers during 7,12-dimethylbenz[a]anthracene-induced hamster buccal pouch carcinogenesis

Silvan, Simon; Manoharan, Shanmugam

doi:10.1016/j.archoralbio.2012.06.005

Cited by 42 publications

(28 citation statements)

References 51 publications

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“…Although angiogenesis is a common phenomenon in physiological conditions, it is also crucial in pathological conditions such as tumor progression and metastasis. Extensive studies reported overexpression of VEGF in oral carcinogenesis (Silvan et al, 2013). Our results are in line with these findings.…”

Section: Discussionsupporting

confidence: 93%

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Anti-cell Proliferative and Anti-angiogenic Potential of Andrographolide During 7,12-Dimethylbenz(a)anthracene Induced Hamster Buccal Pouch Carcinogenesis

Singh

Manoharan²,

Vasudevan³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 93%

“…Over expression of cyclins is one of the common phenomenons of oral cancer (Miyamoto et al, 2003). Overexpression of cyclin D1 was reported in 30-35% of oral carcinogenesis (Sauter et al, 1999;Silvan et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Anti-cell Proliferative and Anti-angiogenic Potential of Andrographolide During 7,12-Dimethylbenz(a)anthracene Induced Hamster Buccal Pouch Carcinogenesis

Singh

Manoharan²,

Vasudevan³

et al. 2013

Asian Pacific Journal of Cancer Prevention

Self Cite

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“…The same research group also showed that apigenin effectively suppressed prostate cancer progression in TRAMP mice by attenuation of insulin-like growth factor (IGF)-I/IGF binding protein-3 signaling and inhibition of angiogenesis and metastasis 15. In addition, a 15-week period of oral administration of apigenin (2.5 mg/kg) in hamsters resulted in reduction of tumor volume and incidence, modulation of cell proliferation, apoptosis, inflammation, and angiogenesis markers, and modulation of phase I and II detoxification cascades in a 7,12-dimethyl benz[ a ]anthracene (DMBA)-induced experimental oral carcinogenesis model 16,17. The chemoprotective effect of apigenin against oral carcinogenesis was further supported by studies reporting that this flavone lowered tumor incidence in DMBA-induced animal model 18,19.…”

Section: Role Of Apigenin In Cancer Preventionmentioning

confidence: 99%

Role of Apigenin in Cancer Prevention via the Induction of Apoptosis and Autophagy

2016

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Apigenin (4′,5,7-trihydroxyflavone) is a flavonoid commonly found in many fruits and vegetables such as parsley, chamomile, celery, and kumquats. In the last few decades, recognition of apigenin as a cancer chemopreventive agent has increased. Significant progress has been made in studying the chemopreventive aspects of apigenin both in vitro and in vivo. Several studies have demonstrated that the anticarcinogenic properties of apigenin occur through regulation of cellular response to oxidative stress and DNA damage, suppression of inflammation and angiogenesis, retardation of cell proliferation, and induction of autophagy and apoptosis. One of the most well-recognized mechanisms of apigenin is the capability to promote cell cycle arrest and induction of apoptosis through the p53-related pathway. A further role of apigenin in chemoprevention is the induction of autophagy in several human cancer cell lines. In this review, we discuss the details of apigenin, apoptosis, autophagy, and the role of apigenin in cancer chemoprevention via the induction of apoptosis and autophagy.

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“…The recent studies involving DMBA-inducted carcinomas in this model [24,28] still use the classic protocols [2,5] for tumor induction. The method described here, associating DMBA with carbamide peroxide, could facilitate the pre-clinic studies on head and neck carcinomas, reducing the laboratory labor and the exposure of the researchers to carcinogenic agents, shortening the time necessary to perform a study, in addition to decrease the costs of experiments involving chemical carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

The Promoting Effect of Carbamide Peroxide Teeth Bleaching Gel in a Preclinical Model of Head and Neck Cancer in Hamster Buccal Pouch

Bampi

Vilela

Gonçalves

et al. 2014

Clin Exp Otorhinolaryngol

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ObjectivesThe aim of this study was to verify the promoting effect of carbamide peroxide on dimethylbenzanthracene (DMBA)-induced carcinogenesis in the hamster buccal pouch, in order to reduce the period of latency for tumor formation.MethodsSixteen hamsters were randomized into two groups of eight animals each. The hamsters of the group I had their right buccal pouches treated with 0.5% DMBA and 10% carbamide peroxide teeth bleaching gel for 55 days. The animals of the group II had their right pouches treated only with DMBA. After, six animals of each group had their pouches prepared for light microscopy. Histomorphometry was performed to assess the presence of keratinization, nuclear polymorphism, pattern of invasion, number of blood vessels, and inflammatory infiltrate in the tumor front. Furthermore, the newly formed lesions were graded according the Bryne's grading system. The remaining animals had the vascular system of the pouches casted by Mercox and qualitatively analyzed by scanning electron microscopy.ResultsHistopathological analysis of the buccal pouches treated with DMBA and carbamide peroxide exhibited formation of squamous cell carcinoma well-differentiated with a high degree of malignancy in all pouches. The development of this neoplasm was associated with a significant increase in the number of blood vessels, presence of keratin pearls, and inflammatory infiltrate. The pouches of the group II showed inflammation, epithelial hyperplasia, dysplasia, and squamous cell carcinoma in only three right pouches. The analysis of the electron micrographs of the pouches chemically inducted with DBMA and carbamide peroxide reveled formation of a new vascular network characteristic of squamous cell carcinoma.ConclusionThe protocol presented here, using DMBA associated with carbamide peroxide, shortens the period of latency to produce squamous cell carcinoma in the hamster buccal pouch, decreasing the time and costs of the experiments.

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Apigenin prevents deregulation in the expression pattern of cell-proliferative, apoptotic, inflammatory and angiogenic markers during 7,12-dimethylbenz[a]anthracene-induced hamster buccal pouch carcinogenesis

Cited by 42 publications

References 51 publications

Anti-cell Proliferative and Anti-angiogenic Potential of Andrographolide During 7,12-Dimethylbenz(a)anthracene Induced Hamster Buccal Pouch Carcinogenesis

Anti-cell Proliferative and Anti-angiogenic Potential of Andrographolide During 7,12-Dimethylbenz(a)anthracene Induced Hamster Buccal Pouch Carcinogenesis

Role of Apigenin in Cancer Prevention via the Induction of Apoptosis and Autophagy

The Promoting Effect of Carbamide Peroxide Teeth Bleaching Gel in a Preclinical Model of Head and Neck Cancer in Hamster Buccal Pouch

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