| Virus Name | Human papillomavirus type 16 |
| Virus Short Name | HPV16 |
| Order | Unassigned |
| Virus Family | Papillomaviridae |
| Virus Subfamily | N.A. |
| Genus | Alphapapillomavirus |
| Species | Human papillomavirus 16 |
| Host | Human, monkeys |
| Cell Tropism | Epithelial cells of skin, mucous membranes |
| Associated Disease | Malignant tumours |
| Mode of Transmission | Sexual, indirect and direct contact, auto-inoculation |
| VIPR DB link | N.A. |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/121/papillomaviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Papillomaviridae |
| Paper Title | Transcription factor AP-1 in esophageal squamous cell carcinoma: alterations in activity and expression during human Papillomavirus infection |
| Author's Name | Showket Hussain, Alok C Bharti, Irfana Salam, Mohammad Akbar Bhat, Mohammad Muzaffar Mir, Suresh Hedau, Mushtaq A Siddiqi, Seemi Farhat Basir and Bhudev C Das |
| Journal Name | BMC Cancer |
| Pubmed ID | 19758438 |
| Abstract | BACKGROUND:Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related deaths in Jammu and Kashmir (J&K) region of India. A substantial proportion of esophageal carcinoma is associated with infection of high-risk HPV type 16 and HPV18, the oncogenic expression of which is controlled by host cell transcription factor Activator Protein-1 (AP-1). We, therefore, have investigated the role of DNA binding and expression pattern of AP-1 in esophageal cancer with or without HPV infection.METHODS:Seventy five histopathologically-confirmed esophageal cancer and an equal number of corresponding adjacent normal tissue biopsies from Kashmir were analyzed for HPV infection, DNA binding activity and expression of AP-1 family of proteins by PCR, gel shift assay and immunoblotting respectively.RESULTS:A high DNA binding activity and elevated expression of AP-1 proteins were observed in esophageal cancer, which differed between HPV positive (19%) and HPV negative (81%) carcinomas. While JunB, c-Fos and Fra-1 were the major contributors to AP-1 binding activity in HPV negative cases, Fra-1 was completely absent in HPV16 positive cancers. Comparison of AP-1 family proteins demonstrated high expression of JunD and c-Fos in HPV positive tumors, but interestingly, Fra-1 expression was extremely low or nil in these tumor tissues.CONCLUSION:Differential AP-1 binding activity and expression of its specific proteins between HPV--positive and HPV--negative cases indicate that AP-1 may play an important role during HPV-induced esophageal carcinogenesis. |
| Used Model | HeLa cells |
| DOI | 10.1186/1471-2407-9-329 |
