scholarly journals Human papillomavirus type 16 circular RNA is barely detectable for the claimed transformation activity

2021 ◽  
Author(s):  
Lulu Yu ◽  
Zhi-Ming Zheng
Keyword(s):  
Human Papillomavirus ◽  
Rna Splicing ◽  
Cell Transformation ◽  
Circular Rna ◽  
Tumor Formation ◽  
Small Interfering Rnas ◽  
E7 Oncoprotein ◽  
Human Papillomavirus Type 16 ◽  
Published Report ◽  
Transformation Activity

The human papillomavirus type 16 (HPV16) E7 oncoprotein plays an essential role in cervical carcinogenesis and is encoded predominantly by a viral E6*I mRNA through alternative RNA splicing of a p97 promoter-transcribed bicistronic E6E7 pre-mRNA. Recently, Zhao et al. detected the HPV16 circular RNA circE7, which is generated aberrantly through backsplicing of the E6E7 pre-mRNA from two HPV16-positive cervical cancer cell lines, CaSki and SiHa. Based on their findings that HPV16 E7 was translated from circE7 and knockdown of circE7 in CaSki cells led to reduction of E7 oncoprotein, cell proliferation, and xenograft tumor formation, the authors claimed that circE7 is functionally important in cell transformation. We believe, however, that the reported circE7 function is overstated. We found that circE7 in CaSki cells is only 0.4 copy per cell and determine that the claimed circE7 function in the published report was resulted from off-targeting viral E7 linear mRNAs by their circE7 small interfering RNAs.

scholarly journals Identification of the FHL2 Transcriptional Coactivator as a New Functional Target of the E7 Oncoprotein of Human Papillomavirus Type 16

2006 ◽  
Vol 81 (2) ◽  
pp. 1027-1032 ◽  
Author(s):  
Beatriz Campo-Fernández ◽  
Dieter Morandell ◽  
Frédéric R. Santer ◽  
Werner Zwerschke ◽  
Pidder Jansen-Dürr
Keyword(s):  
Human Papillomavirus ◽  
Zinc Finger ◽  
Cell Transformation ◽  
Zinc Finger Domain ◽  
Transcriptional Coactivator ◽  
Hpv 16 ◽  
E7 Oncoprotein ◽  
Human Papillomavirus Type 16 ◽  
Conserved Regions ◽  
Novel Target

ABSTRACT We identified the transcriptional coactivator FHL2 as a novel target of the human papillomavirus type 16 (HPV-16) E7 oncoprotein, which plays a major role in cell transformation. The interaction with FHL2 is abolished by mutations in conserved regions 1 and 2 and in the C-terminal zinc finger domain of E7, all required for its transforming potential. We found that E7 impairs the coactivator function of FHL2 on both β-catenin/LCF-dependent and AP-1-dependent promoters. Thus, the interaction with HPV-16 E7 leads to a promoter-specific impairment of FHL2 function and this may contribute to cell transformation.

scholarly journals Structure-function analysis of the human papillomavirus type 16 E7 oncoprotein.

1992 ◽  
Vol 66 (4) ◽  
pp. 2418-2427 ◽  
Author(s):  
W C Phelps ◽  
K Münger ◽  
C L Yee ◽  
J A Barnes ◽  
P M Howley
Keyword(s):  
Human Papillomavirus ◽  
Structure Function ◽  
Function Analysis ◽  
E7 Oncoprotein ◽  
Human Papillomavirus Type 16

scholarly journals Cervical Cancers Require the Continuous Expression of the Human Papillomavirus Type 16 E7 Oncoprotein Even in the Presence of the Viral E6 Oncoprotein

2012 ◽  
Vol 72 (16) ◽  
pp. 4008-4016 ◽  
Author(s):  
Sean F. Jabbar ◽  
Soyeong Park ◽  
Johannes Schweizer ◽  
Marthe Berard-Bergery ◽  
Henry C. Pitot ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Cervical Cancers ◽  
E7 Oncoprotein ◽  
Human Papillomavirus Type 16 ◽  
E6 Oncoprotein

Human Papillomavirus Type 16 E7 Oncoprotein Binds and Inactivates Growth-Inhibitory Insulin-Like Growth Factor Binding Protein 3

2000 ◽  
Vol 20 (17) ◽  
pp. 6483-6495
Author(s):  
Boris Mannhardt ◽  
Stuart A. Weinzimer ◽  
Mechthild Wagner ◽  
Marc Fiedler ◽  
Pinchas Cohen ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Growth Factor ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
E7 Oncoprotein ◽  
Human Papillomavirus Type 16 ◽  
Growth Inhibitory

scholarly journals Stabilization and Functional Impairment of the Tumor Suppressor p53 by the Human Papillomavirus Type 16 E7 Oncoprotein

Virology ◽  
2002 ◽  
Vol 295 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Alexandra Eichten ◽  
Matthew Westfall ◽  
Jennifer A. Pietenpol ◽  
Karl Münger
Keyword(s):  
Human Papillomavirus ◽  
Tumor Suppressor ◽  
Functional Impairment ◽  
Tumor Suppressor P53 ◽  
E7 Oncoprotein ◽  
Human Papillomavirus Type 16

scholarly journals Human Papillomavirus Type 16 E7 Oncoprotein Associates with the Centrosomal Component γ-Tubulin

2007 ◽  
Vol 81 (24) ◽  
pp. 13533-13543 ◽  
Author(s):  
Christine L. Nguyen ◽  
Catherine Eichwald ◽  
Max L. Nibert ◽  
Karl Münger
Keyword(s):  
Human Papillomavirus ◽  
Gradient Centrifugation ◽  
Sucrose Density Gradient ◽  
Sucrose Density Gradient Centrifugation ◽  
E7 Oncoprotein ◽  
Human Papillomavirus Type 16 ◽  
Retinoblastoma Tumor Suppressor ◽  
Mitotic Abnormalities ◽  
Small Pool ◽  
Retinoblastoma Tumor

ABSTRACT Expression of a high-risk human papillomavirus (HPV) E7 oncoprotein is sufficient to induce aberrant centrosome duplication in primary human cells. The resulting centrosome-associated mitotic abnormalities have been linked to the development of aneuploidy. HPV type 16 (HPV16) E7 induces supernumerary centrosomes through a mechanism that is at least in part independent of the inactivation of the retinoblastoma tumor suppressor pRb and is dependent on cyclin-dependent kinase 2 activity. Here, we show that HPV16 E7 can concentrate around mitotic spindle poles and that a small pool of HPV16 E7 is associated with centrosome fractions isolated by sucrose density gradient centrifugation. The targeting of HPV16 E7 to the centrosome, however, was not sufficient for centrosome overduplication. Nonetheless, we found that HPV16 E7 can associate with the centrosomal regulator γ-tubulin and that the recruitment of γ-tubulin to the centrosome is altered in HPV16 E7-expressing cells. Since the association of HPV16 E7 with γ-tubulin is independent of pRb, p107, and p130, our results suggest that the association with γ-tubulin contributes to the pRb/p107/p130-independent ability of HPV16 E7 to subvert centrosome homeostasis.

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