Immortalization of primary rat cells by human papillomavirus type 16 subgenomic DNA fragments controlled by the SV40 promoter

Kanda, Tadahito; Watanabe, Shiro; Yoshiike, Kunito

doi:10.1016/0042-6822(88)90694-0

Cited by 111 publications

(64 citation statements)

References 30 publications

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“…Expression of the viral proteins E6 and E7 by a subset of HPV can immortalize infected cells and then may later ensure progression to malignant disease (1,2). HPV strain 16 is associated with Ͼ50% of cervical cancer cases (3)(4)(5).…”

Section: H Uman Papilloma Viruses (Hpv)mentioning

confidence: 99%

Two Listeria monocytogenes Vaccine Vectors That Express Different Molecular Forms of Human Papilloma Virus-16 (HPV-16) E7 Induce Qualitatively Different T Cell Immunity That Correlates with Their Ability to Induce Regression of Established Tumors Immortalized by HPV-16

Gunn

Zubair

Peters

et al. 2001

The Journal of Immunology

271

309

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Two recombinant Listeria monocytogenes (rLm) strains were produced that secrete the human papilloma virus-16 (HPV-16) E7 protein expressed in HPV-16-associated cervical cancer cells. One, Lm-E7, expresses and secretes E7 protein, whereas a second, Lm-LLO-E7, secretes E7 as a fusion protein joined to a nonhemolytic listeriolysin O (LLO). Lm-LLO-E7, but not Lm-E7, induces the regression of the E7-expressing tumor, TC-1, established in syngeneic C57BL/6 mice. Both recombinant E7-expressing rLm vaccines induce measurable anti-E7 CTL responses that stain positively for H-2Db E7 tetramers. Depletion of the CD8+ T cell subset before treatment abrogates the ability of Lm-LLO-E7 to impact on tumor growth. In addition, the rLm strains induce markedly different CD4+ T cell subsets. Depletion of the CD4+ T cell subset considerably reduces the ability of Lm-LLO-E7 to eliminate established TC-1 tumors. Surprisingly, the reverse is the case for Lm-E7, which becomes an effective anti-tumor immunotherapeutic in mice lacking this T cell subset. Ab-mediated depletion of TGF-β and CD25+ cells improves the effectiveness of Lm-E7 treatment, suggesting that TGF-β and CD25+ cells are in part responsible for this suppressive response. CD4+ T cells from mice immunized with Lm-E7 are capable of suppressing the ability of Lm-LLO-E7 to induce the regression of TC-1 when transferred to tumor-bearing mice. These studies demonstrate the complexity of L. monocytogenes-mediated tumor immunotherapy targeting the human tumor Ag, HPV-16 E7.

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Section: H Uman Papilloma Viruses (Hpv)mentioning

confidence: 99%

Two Listeria monocytogenes Vaccine Vectors That Express Different Molecular Forms of Human Papilloma Virus-16 (HPV-16) E7 Induce Qualitatively Different T Cell Immunity That Correlates with Their Ability to Induce Regression of Established Tumors Immortalized by HPV-16

Gunn

Zubair

Peters

et al. 2001

The Journal of Immunology

271

309

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“…ras) leads to immortalization of primary rodent cells (Chesters and McCance, 1989;Crook et al, 1991a;Liu et al, 1994;Peacock et al, 1990;Phelps et al, 1988;Storey and Banks, 1993;Storey et al, 1988). The expression of either the E6 or E7 genes is also sucient to transform immortalized rodent cells (Bedell et al, 1989;Kanda et al, 1988;Sedman et al, 1991;Tanaka et al, 1989;Vousden et al, 1988). Finally, the combined expression of E6 and E7 eciently immortalizes primary human keratinocytes (Barbosa and Schlegel, 1989;HawleyNelson et al, 1989;Hudson et al, 1990;MuÈ nger et al, 1989;Sedman et al, 1991), although it does not induce directly the tumorigenic phenotype.…”

Section: Introductionmentioning

confidence: 99%

The E7 protein of human papillomavirus type 16 sensitizes primary human keratinocytes to apoptosis

Stöppler

Johnson

et al. 1998

Oncogene

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The`high risk' human papillomaviruses are associated with the development of anogenital carcinomas and their E6 and E7 genes possess immortalizing and transforming functions in several in vitro culture systems. Recently the E6 gene has also been shown to enhance the apoptosis of human mammary epithelial cells. To determine the apoptotic activity of these oncogenes in the natural host cell, we infected genital keratinocytes with retroviruses expressing either HPV-16 E6, E7, or both the E6 and E7 (E6/7) genes. Apoptosis was quantitated under normal growth conditions or when induced by tumor necrosis factor a/cycloheximide or sulfur mustard. In contrast to previous ®ndings with mammary epithelial cells, the E6 gene did not signi®cantly augment either spontaneous or induced apoptosis. E6 also did not suppress apoptosis in normal keratinocytes (despite dramatically reducing their p53 levels), suggesting that p53-independent events mediated this eect. In contrast, E7 increased both spontaneous and induced apoptosis as well as the cellular levels of p53 and p21 protein. Interestingly, coexpression of E6 abrogated E7-facilitated apoptosis by tumor necrosis factor a nearly completely, but had only a minor protective eect on sulfur mustard induced apoptosis in these cells, demonstrating at least in part the p53-dependence and -independence of these two apoptotic pathways. Finally, our results indicate that the apoptosis of normal and E7-expressing keratinocytes is dierentially aected by E6 expression and that E7, when unaccompanied by E6, sensitizes keratinocytes to apoptosis.

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“…A property which ElA proteins share with the simian virus 40 (SV40) large T antigen (LT Ag), the large T antigen of polyomavirus, and the E7 gene of human papillomavirus 16 (HPV16) is the ability to establish continuous in vitro proliferation of primary cells (24,29,47,48,50,51). Moreover, these same viral proteins have also been shown to associate with the RB1 protein (8,9,63).…”

mentioning

confidence: 99%

Maintenance of cellular proliferation by adenovirus early region 1A in fibroblasts conditionally immortalized by using simian virus 40 large T antigen requires conserved region 1.

Riley¹,

Follin²,

Jones³

et al. 1990

Mol. Cell. Biol.

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Various mutants of adenovirus E1A were assayed for their ability to complement the growth defect at the nonpermissive temperature for the cell line tsa14 which was isolated by immortalizing rat embryo fibroblasts with the thermolabile large T antigen of tsA58. This cell line grows indefinitely at the permissive temperature but undergoes rapid growth arrest upon shift up to the nonpermissive temperature. Since this growth arrest can be overcome by introduction of wild-type simian virus 40 large T antigen, human papillomavirus 16 E7, and adenovirus E1A, the tsa14 cells provided an excellent system for defining regions of E1A necessary for complementation of the growth defect. We demonstrate that conserved region 1 (CR1) is the region of E1A required for complementation. While CR2 of E1A has been shown to be required for the immortalization of primary cells and is also necessary for the binding of the 105-kDa retinoblastoma protein, mutations within this region did not abrogate complementation of the growth defect. However, since both CR1 and CR2 have previously been shown to be absolutely required for immortalization of primary cells by adenovirus E1A, this evidence suggests that the tsa14 system assays for the maintenance of proliferation and that this requires CR1.

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Immortalization of primary rat cells by human papillomavirus type 16 subgenomic DNA fragments controlled by the SV40 promoter

Cited by 111 publications

References 30 publications

Two Listeria monocytogenes Vaccine Vectors That Express Different Molecular Forms of Human Papilloma Virus-16 (HPV-16) E7 Induce Qualitatively Different T Cell Immunity That Correlates with Their Ability to Induce Regression of Established Tumors Immortalized by HPV-16

Two Listeria monocytogenes Vaccine Vectors That Express Different Molecular Forms of Human Papilloma Virus-16 (HPV-16) E7 Induce Qualitatively Different T Cell Immunity That Correlates with Their Ability to Induce Regression of Established Tumors Immortalized by HPV-16

The E7 protein of human papillomavirus type 16 sensitizes primary human keratinocytes to apoptosis

Maintenance of cellular proliferation by adenovirus early region 1A in fibroblasts conditionally immortalized by using simian virus 40 large T antigen requires conserved region 1.

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