Association between areca‐stimulated vimentin expression and the progression of head and neck cancers

Tseng, Yu‐Hsin; Chang, Kuo Wei; Yang, Cheng Chieh; Liu, Chung Ji; Liu, Tsung Yun; Lin, Shu Chun

doi:10.1002/hed.21726

Cited by 8 publications

(7 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tumors exhibiting no vimentin expression and weak AKT phosphorylation were found to be associated with better survival than groups with higher levels of expression. These results imply that PI3K/AKT activation and vimentin expression are important pathogenic cascades in BN associated OC [171]. It thus appears that there is conclusive evidence to support a role of increased expression of vimentin in BN associated carcinogenesis [170], [171].…”

Section: Resultsmentioning

confidence: 71%

“…These results imply that PI3K/AKT activation and vimentin expression are important pathogenic cascades in BN associated OC [171]. It thus appears that there is conclusive evidence to support a role of increased expression of vimentin in BN associated carcinogenesis [170], [171]. Involucrin is a key component of the cornified envelope and a differentiation marker of keratinocytes.…”

Section: Resultsmentioning

confidence: 80%

See 1 more Smart Citation

Association of Betel Nut with Carcinogenesis: Revisit with a Clinical Perspective

et al. 2012

View full text Add to dashboard Cite

Betel nut (BN), betel quid (BQ) and products derived from them are widely used as a socially endorsed masticatory product. The addictive nature of BN/BQ has resulted in its widespread usage making it the fourth most abused substance by humans. Progressively, several additives, including chewing tobacco, got added to simple BN preparations. This addictive practice has been shown to have strong etiological correlation with human susceptibility to cancer, particularly oral and oropharyngeal cancers.The PUBMED database was searched to retrieve all relevant published studies in English on BN and BQ, and its association with oral and oropharyngeal cancers. Only complete studies directly dealing with BN/BQ induced carcinogenesis using statistically valid and acceptable sample size were analyzed. Additional relevant information available from other sources was also considered.This systematic review attempts to put in perspective the consequences of this widespread habit of BN/BQ mastication, practiced by approximately 10% of the world population, on oral cancer with a clinical perspective. BN/BQ mastication seems to be significantly associated with susceptibility to oral and oropharyngeal cancers. Addition of tobacco to BN has been found to only marginally increase the cancer risk. Despite the widespread usage of BN/BQ and its strong association with human susceptibility to cancer, no serious strategy seems to exist to control this habit. The review, therefore, also looks at various preventive efforts being made by governments and highlights the multifaceted intervention strategies required to mitigate and/or control the habit of BN/BQ mastication.

show abstract

Section: Resultsmentioning

confidence: 71%

Section: Resultsmentioning

confidence: 80%

Association of Betel Nut with Carcinogenesis: Revisit with a Clinical Perspective

et al. 2012

View full text Add to dashboard Cite

show abstract

“…The activation of caspase-3 and enhanced PARP-cleavage further validated the apoptosis observed by TUNEL apoptosis assay following didymin treatment. The expression of vimentin is associated with enhanced motility of tumor cells and hence inhibition of vimentin by didymin was significant in the context of anti-migratory effects of didymin in neuroblastomas as revealed by in vitro migration assay (26, 27). Thus, these results provided further corroborative evidence for the observed anti-proliferative and pro-apoptotic effects of didymin in initial cell survival, clonogenic and apoptosis studies.…”

Section: Resultsmentioning

confidence: 99%

Didymin Induces Apoptosis by Inhibiting N-Myc and Upregulating RKIP in Neuroblastoma

Singhal

Nagaprashantha²,

Vatsyayan³

et al. 2012

Cancer Prevention Research

View full text Add to dashboard Cite

Neuroblastomas arise from the neural crest cells and represent the most common solid tumors outside the nervous system in children. The amplification of N-Myc plays a primary role in the pathogenesis of neuroblastomas whereas acquired mutations of p53 lead to refractory and relapsed cases of neuroblastomas. In this regard, dietary compounds which can target N-Myc and exert anti-cancer effects independent of p53 status acquire significance in the management of neuroblastomas. Hence, we investigated the anti-cancer properties of the flavonoid didymin in neuroblastomas. Didymin effectively inhibited proliferation and induced apoptosis irrespective of p53 status in neuroblastomas. Didymin down regulated PI3K, pAkt, Akt, vimentin and up regulated RKIP levels. Didymin induced G2/M arrest along with decreasing the levels of cyclin D1, CDK4 and cyclin B1. Importantly, didymin inhibited NMyc as confirmed at protein, mRNA and transcriptional level by promoter-reporter assays. HPLC analysis of didymin (2 mg/kg b.w.) treated mice serum revealed effective oral absorption with free didymin concentration of 2.1 μM. Further in vivo mice xenograft studies revealed that didymin (2 mg/kg b.w.) treated animals had significant reductions in tumors size compared to controls. Didymin strongly inhibited the proliferation (Ki67) and angiogenesis (CD31) markers as well as N-Myc expression as revealed by the histopathological examination of paraffin embedded section of resected tumors. Collectively, our in vitro and in vivo studies elucidated the anti-cancer properties and mechanisms of action of a novel, orally active and palatable flavonoid didymin which makes it a potential new approach for neuroblastoma therapy (NANT) to target pediatric neuroblastomas.

show abstract

“…The increased cell motility was regulated via the activation of Src and ERK kinases . In both clinical and cellular model, investigations showed the association of areca‐stimulated vimentin expression, cell mobility, and progression of OSCC, implying tumorigenic effect of ANE could be through regulation of cytoskeletal proteins . Moreover, elevated content of metal ion copper in the areca nut was detected in OSF tissues, supporting the idea that copper is an initiating factor for OSF while this pathological fibrogenic stimulation may be mediated by the up‐regulation of lysyl oxidase (LOX) activity .…”

Section: Areca (Betel) Nut Chewing Vs Oral Carcinogenesismentioning

confidence: 84%

Molecular and cellular cues of diet‐associated oral carcinogenesis—with an emphasis on areca‐nut‐induced oral cancer development

Li¹,

Lee²,

Chou

et al. 2014

J Oral Pathology Medicine

Self Cite

View full text Add to dashboard Cite

In modern times, potent dietary carcinogens are key contributors for neoplastic development. For oral squamous cell carcinoma (OSCC), one of the leading cancer types in developing countries, main oncogenic inducers/enhancers, including areca nut chewing, tobacco smoking, and alcohol consumption, were shown to promote cancer initiation/progression. Over decades, studies from different laboratories have identified underlying cellular and molecular mechanisms for carcinogen-induced OSCC. In this review, we will give an overview of where we are in understanding potential oral carcinogenic factors stimulated OSCC tumorigenesis, especially those associated with areca nut chewing in Asians, aiming to provide future scope of possible interception.

show abstract

Association between areca‐stimulated vimentin expression and the progression of head and neck cancers

Abstract: Areca-modulated vimentin expression enhanced the progression of head and neck carcinoma.

Cited by 8 publications

References 22 publications

Association of Betel Nut with Carcinogenesis: Revisit with a Clinical Perspective

Association of Betel Nut with Carcinogenesis: Revisit with a Clinical Perspective

Didymin Induces Apoptosis by Inhibiting N-Myc and Upregulating RKIP in Neuroblastoma

Molecular and cellular cues of diet‐associated oral carcinogenesis—with an emphasis on areca‐nut‐induced oral cancer development

Contact Info

Product

Resources

About