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Cell Journal، جلد ۱۳، شماره Supplement، صفحات ۰-۰
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عنوان انگلیسی EBV and HPV Infection in Nasopharyngeal Cancer in Relation to Cell Cycle Regulatory and Apoptotic Proteins
چکیده انگلیسی مقاله Nasopharyngeal carcinoma (NPC) is a malignancy of the nasal epithelium, 70-80% of which is associated with Epstein Barr virus (EBV) infection and has characteristic features of high sensitivity to radiation therapy. However, the high mortality rate is associated with the high recurrence rate in these patients. Infection by human papilloma virus (HPV) has been reported in 20-30% of these cancers. Viral proteins have been described to influence the behaviour of tumour cells. Studies into the proteins involved and their targets would be beneficial in manipulating treatment strategies for a better control of the tumour. The cell cycle proteins are the most important effectors of cell growth and a negative regulation of these proteins by exogenous proteins can lead to their malfunctioning and thereby carcinogenesis. EBV and HPV proteins have been studied for their interaction with cellular proteins. As much as 173 interactions between EBV and human proteins have been identified. Studies on the influence of EBV and HPV proteins on survival and response to treatment in NPC is scanty. An increased radio-resistance of HPV positive NPCs was reported by us while the EBV positive NPCs were radiosensitive, the mechanisms responsible for this difference remain vague. Our studies showed that HPV and EBV had differential effects on the expression of some of the important cell cycle regulatory proteins. EBV infection had no significant effect on the cell cycle regulatory proteins except for a reduction in p16, but showed significantly increased expression of anti-apoptotic protein Bcl2. This was in contrast to an increased expression of proliferation associated proteins and no effect on apoptotic proteins in HPV +ve tumours. The results clearly showed that the two viruses utilise different pathways in deregulating cell proliferation in NPC. The EBV mainly brings about an imbalance in the proliferation/apoptosis balance by upregulating Bcl2 while HPV infection upregulates proliferation along with the concomitant increase in apoptosis without affecting the apoptotic proteins. The downregulation of p27 in HPV +ve tumours and p16 in EBV+ve tumours again point towards the utilisation of different pathways by the two viruses in NPC carcinogenesis.
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نشانی اینترنتی http://celljournal.org/journal/article/abstract/1485
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