The E7 gene of human papillomavirus type 16 is sufficient for immortalization of human epithelial cells

Abstract

The contribution of the E6 and E7 open reading frames of human papillomavirus type 6b (HPV6b) and HPV16 to immortalization of human keratinocytes was evaluated by using amphotropic recombinant retroviruses. The HPV16 E7 gene could immortalize primary human keratinocytes without the cooperation of the viral E6 gene; however, E6 was able to contribute significantly to the efficiency of the E7 immortalizing function. Infection of HFE cells with retroviruses carrying the 16E6, 6bE6, 6bE7, or 6bE6E7 open reading frame did not result in immortalization.

Class III β‐tubulin, a marker of resistance to paclitaxel, is overexpressed in pancreatic ductal adenocarcinoma and intraepithelial neoplasia

“…The retroviral vectors employed (pLXSN-E6 ⁄ E7, pBabe Hygro ras) have been described previously. 26,27 Amphotropic viruses were collected following transient transfection of phoenix A packaging cells. Transient transfections were performed with calcium phosphate using a commercial kit (MBS kit; Stratagene).…”

Immortalisation of human bone marrow endothelial cells: characterisation of new cell lines

“…HBMEC were immortalised with the use of the amphotrophic helper-free retrovirus pLXSN16E6/E7 [13], as described previously [24]. The packaging cell line PA317, which produces the amphotrophic helper-free retrovirus pLXSN16E6/E7 [17], was kindly provided by Dr D. A. Galloway (Fred Hutchinson Cancer Research Center, Seattle, WA, USA).…”

“…To overcome these problems, we have immortalised primary HBMEC. In contrast to three previously described HBMEC cell lines, which were all immortalised by the introduction of the simian virus (SV40) large T antigen [10±12], we used a retroviral construct pLXSN16 E6/E7 [13]. This amphotrophic, replication-defective retroviral construct contains the E6/E7 genes from the human papilloma virus 16 (HPV16).…”

Two enemies, one fight: An update of oral cancer in patients with Fanconi anemia

“…91 In virus-infected cells, E6 and E7 inactivate 2 tumor suppressors (p53 and pRb) and induce carcinogenesis. 92,93 Studies suggest an interaction between HPV and the FA pathway. In tissue culture, HPV16 E7 stimulates transcription of FANCD2 and activates the FA/BRCA pathway.…”