Analysis of apoptosis‐associated genes and pathways in oral cancer cells

Gibson, Sandra; Shillitoe, Edward J.

doi:10.1111/j.1600-0714.2006.00398.x

Cited by 11 publications

(10 citation statements)

References 35 publications

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“…Recently, it has been demonstrated that NME5 was downregulated in several tumor types, including immortalized human urothelial cells, urothelial carcinoma and primary urothelial tumors through microarray (Chapman et al, 2008). However, NME5 gene expression in human oral cancer cell line Tu183 was constitutively higher than that in normal human epidermal keratinocyte cells (Gibson and Shillitoe, 2006). To date, many research concerning the expression and/or the role of NME5 in human pancreatic cancer have seldom been reported.…”

Section: Introductionmentioning

confidence: 98%

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Jiang

Wang

et al. 2012

Gene

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Section: Introductionmentioning

confidence: 98%

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Jiang

Wang

et al. 2012

Gene

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“…In recent years, it has been known that a serial changes in the process of apoptosis is also an essential feature of cancer cells (Gibson and Shillitoe, 2006). Apoptotic process involves an intricate cascade of events which is highly regulated (Malaguarnera et al, 2012;Ko et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Expression of Survivin and Caspase 3 in Oral Squamous Cell Carcinoma and Peritumoral Tissue

Li¹,

Chai²,

Cai³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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This study was conducted to investigate the expression of survivin and caspase 3 in oral squamous cell carcinoma and peritumoral tissue, and possible pathogenesis mechanisms. We used ELISA and western blotting to detect the protein expression levels of survivin and caspase 3 in tissue. In situ hybridization and real-time PCR were applied to assess mRNA expression levels. In this study, 13 tumor samples and 13 peritumoral tissue samples were collected from oral squamous cell carcinoma patients and 10 normal tissue samples obtained from patients without tumor. The result showed that the protein and mRNA expression of survivin in carcinoma was the highest among three types of tissue; following was that in peritumoral tissue. No difference in caspase 3 zymogen between peritumoral tissue and normal tissue could be found, while it was evidently decreased in carcinoma tissue. Activated caspase 3 was detected in normal tissue but could not be identified in peritumoral or carcinoma tissue. Our results indicate that the expression of survivin is apparently elevated in tumoral and peritumoral tissue. Expression of activated caspase 3 was not detected in tumoral tissue and the expression of caspase 3 zymogen was decreased in tumoral tissue. Our findings suggest that survivin may inhibit both synthesis and activation of caspase 3, hence inhibiting cell apoptosis and facililitating eventual development of oral squamous cell carcinoma.

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“…Moreover, oral cancer cells (e.g., Tu183 cells) are known to adapt genetic changes that block cell death. Examples of such adaptations include mutations of p53 and upregulation of bcl -2 expression [12] . …”

Section: Discussionmentioning

confidence: 99%

“…Tu183 cells are derived from a squamous cell carcinoma of the tonsil [11] . This epithelial cell line overexpresses bcl-2 and is highly resistant to cytotoxic drugs [12][13][14][15] .…”

mentioning

confidence: 99%

Cannabinoids Inhibit Cellular Respiration of Human Oral Cancer Cells

et al. 2010

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Background and Purpose: The primary cannabinoids, Δ⁹-tetrahydrocannabinol (Δ⁹-THC) and Δ⁸-tetrahydrocannabinol (Δ⁸-THC) are known to disturb the mitochondrial function and possess antitumor activities. These observations prompted us to investigate their effects on the mitochondrial O₂ consumption in human oral cancer cells (Tu183). This epithelial cell line overexpresses bcl-2 and is highly resistant to anticancer drugs. Experimental Approach: A phosphorescence analyzer that measures the time-dependence of O₂ concentration in cellular or mitochondrial suspensions was used for this purpose. Key Results: A rapid decline in the rate of respiration was observed when Δ⁹-THC or Δ⁸-THC was added to the cells. The inhibition was concentration-dependent, and Δ⁹-THC was the more potent of the two compounds. Anandamide (an endocannabinoid) was ineffective; suggesting the effects of Δ⁹-THC and Δ⁸-THC were not mediated by the cannabinoidreceptors. Inhibition of O₂ consumption by cyanide confirmed the oxidations occurred in the mitochondrial respiratory chain. Δ⁹-THC inhibited the respiration of isolated mitochondria from beef heart. Conclusions and Implications: These results show the cannabinoids are potent inhibitors of Tu183 cellular respiration and are toxic to this highly malignant tumor.

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Analysis of apoptosis‐associated genes and pathways in oral cancer cells

Abstract: The effects of different apoptotic stimuli on normal cells and oral cancer cells can be explained by expression of proapoptosis genes, including the gene that encodes CD40.

Cited by 11 publications

References 35 publications

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells

Expression of Survivin and Caspase 3 in Oral Squamous Cell Carcinoma and Peritumoral Tissue

Cannabinoids Inhibit Cellular Respiration of Human Oral Cancer Cells

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