Downregulation of Ches1 and other novel genes in oral cancer cells chronically exposed to areca nut extract

Yin Ju Chen; Chun Ta Liao; Po Jen Chen; Li Yu Lee; Yi Chen Li; I. How Chen; Hung Ming Wang; Joseph T. Chang; Li Ju Chen; Tzu Chen Yen; Chuan Yi Tang; Ann Joy Cheng

doi:10.1002/hed.21442

Downregulation of Ches1 and other novel genes in oral cancer cells chronically exposed to areca nut extract

Yin Ju Chen, Chun Ta Liao, Po Jen Chen, Li Yu Lee, Yi Chen Li, I. How Chen, Hung Ming Wang, Joseph T. Chang, Li Ju Chen, Tzu Chen Yen, Chuan Yi Tang, Ann Joy Cheng

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

Abstract

Background This study was undertaken to identify the genes in response to areca nut extract, a potential carcinogen of oral cancer. Methods Two oral cancer sublines chronically treated with areca nut extract were established. Methods such as microarray and immunohistochemistry were used to screen and validate the genes' altered expressions in areca nut extract-sublines or in cancer tissues. Results A total of 35 genes were differentially expressed in both sublines. Several functional pathways were significantly altered. Six genes were confirmed over 2-fold of changes, including Ches1. Functional analyses showed that overexpression of Ches1 suppressed cell growth and arrested cells in the G2/M phase. Consistently, this gene has reduced expression in 52% of oral cancer tissues, which was significantly correlated with the areca nut chewing habit of patients (p =.04). Conclusion We identified 35 candidates and validated 6 genes that may be associated with areca nut-induced oral cancer. Loss of Ches1 may be attributed to areca nut extract-induced oral carcinogenesis.

Original language	English
Pages (from-to)	257-266
Number of pages	10
Journal	Head and Neck
Volume	33
Issue number	2
DOIs	https://doi.org/10.1002/hed.21442
Publication status	Published - Feb 2011

Keywords

Ches1
areca nut
clinical association
growth suppression
oral cancer

ASJC Scopus subject areas

Otorhinolaryngology

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10.1002/hed.21442

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Downregulation of Ches1 and other novel genes in oral cancer cells chronically exposed to areca nut extract. / Chen, Yin Ju; Liao, Chun Ta; Chen, Po Jen; Lee, Li Yu; Li, Yi Chen; Chen, I. How; Wang, Hung Ming; Chang, Joseph T.; Chen, Li Ju; Yen, Tzu Chen; Tang, Chuan Yi; Cheng, Ann Joy.

In: Head and Neck, Vol. 33, No. 2, 02.2011, p. 257-266.

Research output: Contribution to journal › Article › peer-review

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abstract = "Background This study was undertaken to identify the genes in response to areca nut extract, a potential carcinogen of oral cancer. Methods Two oral cancer sublines chronically treated with areca nut extract were established. Methods such as microarray and immunohistochemistry were used to screen and validate the genes' altered expressions in areca nut extract-sublines or in cancer tissues. Results A total of 35 genes were differentially expressed in both sublines. Several functional pathways were significantly altered. Six genes were confirmed over 2-fold of changes, including Ches1. Functional analyses showed that overexpression of Ches1 suppressed cell growth and arrested cells in the G2/M phase. Consistently, this gene has reduced expression in 52% of oral cancer tissues, which was significantly correlated with the areca nut chewing habit of patients (p =.04). Conclusion We identified 35 candidates and validated 6 genes that may be associated with areca nut-induced oral cancer. Loss of Ches1 may be attributed to areca nut extract-induced oral carcinogenesis.",

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author = "Chen, {Yin Ju} and Liao, {Chun Ta} and Chen, {Po Jen} and Lee, {Li Yu} and Li, {Yi Chen} and Chen, {I. How} and Wang, {Hung Ming} and Chang, {Joseph T.} and Chen, {Li Ju} and Yen, {Tzu Chen} and Tang, {Chuan Yi} and Cheng, {Ann Joy}",

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AU - Chen, I. How

AU - Wang, Hung Ming

AU - Chang, Joseph T.

AU - Chen, Li Ju

AU - Yen, Tzu Chen

AU - Tang, Chuan Yi

AU - Cheng, Ann Joy

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N2 - Background This study was undertaken to identify the genes in response to areca nut extract, a potential carcinogen of oral cancer. Methods Two oral cancer sublines chronically treated with areca nut extract were established. Methods such as microarray and immunohistochemistry were used to screen and validate the genes' altered expressions in areca nut extract-sublines or in cancer tissues. Results A total of 35 genes were differentially expressed in both sublines. Several functional pathways were significantly altered. Six genes were confirmed over 2-fold of changes, including Ches1. Functional analyses showed that overexpression of Ches1 suppressed cell growth and arrested cells in the G2/M phase. Consistently, this gene has reduced expression in 52% of oral cancer tissues, which was significantly correlated with the areca nut chewing habit of patients (p =.04). Conclusion We identified 35 candidates and validated 6 genes that may be associated with areca nut-induced oral cancer. Loss of Ches1 may be attributed to areca nut extract-induced oral carcinogenesis.

AB - Background This study was undertaken to identify the genes in response to areca nut extract, a potential carcinogen of oral cancer. Methods Two oral cancer sublines chronically treated with areca nut extract were established. Methods such as microarray and immunohistochemistry were used to screen and validate the genes' altered expressions in areca nut extract-sublines or in cancer tissues. Results A total of 35 genes were differentially expressed in both sublines. Several functional pathways were significantly altered. Six genes were confirmed over 2-fold of changes, including Ches1. Functional analyses showed that overexpression of Ches1 suppressed cell growth and arrested cells in the G2/M phase. Consistently, this gene has reduced expression in 52% of oral cancer tissues, which was significantly correlated with the areca nut chewing habit of patients (p =.04). Conclusion We identified 35 candidates and validated 6 genes that may be associated with areca nut-induced oral cancer. Loss of Ches1 may be attributed to areca nut extract-induced oral carcinogenesis.

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