scholarly journals Inhibition of Serum- and Calcium-Induced Differentiation of Human Keratinocytes by HPV16 E6 Oncoprotein: Role of p53 Inactivation

Virology ◽  
1997 ◽  
Vol 237 (2) ◽  
pp. 296-306 ◽  
Author(s):  
Levana Sherman ◽  
Anna Jackman ◽  
Hagar Itzhaki ◽  
Melissa Conrad Stöppler ◽  
Debbie Koval ◽  
...  
2008 ◽  
Vol 154 (1) ◽  
pp. 55-63 ◽  
Author(s):  
Alexander Epshtein ◽  
A. Jackman ◽  
P. Gonen ◽  
L. Sherman

Virology ◽  
1999 ◽  
Vol 257 (2) ◽  
pp. 383-396 ◽  
Author(s):  
Jacklin Alfandari ◽  
Sharon Shnitman Magal ◽  
Anna Jackman ◽  
Richard Schlegel ◽  
Pinhas Gonen ◽  
...  

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mei-Zhen Dai ◽  
Yi Qiu ◽  
Xing-Hong Di ◽  
Wei-Wu Shi ◽  
Hui-Hui Xu

Abstract Background Human papillomavirus (HPV) type 16 accounts for a larger share of cervical cancer and has been a major health problem worldwide for decades. The progression of initial infection to cervical cancer has been linked to viral sequence properties; however, the role of HPV16 variants in the risk of cervical carcinogenesis, especially with longitudinal follow-up, is not fully understood in China. Methods We aimed to investigate the genetic variability of HPV16 E6 and E7 oncogenes in isolates from cervical exfoliated cells. Between December 2012 and December 2014, a total of 310 single HPV16-positive samples were selected from women living in the Taizhou area, China. Sequences of all E6 and E7 oncogenes were analysed by PCR-sequencing assay. Detailed sequence comparison, genetic heterogeneity analyses and maximum-likelihood phylogenetic tree construction were performed with BioEdit Sequence Alignment Editor and MEGA X software. Data for cytology tests and histological diagnoses were obtained from our Taizhou Area Study with longitudinal follow-up for at least 5 years. The relationship between HPV16 variants and cervical carcinogenesis risk was analysed by the chi-square test or Fisher’s exact test. Results In this study, we obtained 64 distinct variation patterns with the accession GenBank numbers MT681266-MT681329. Phylogenetic analysis revealed that 98.3% of HPV16 variants belong to lineage A, in which the A4 (Asian) sublineage was dominant (64.8%), followed by A2 (12.1%), A1 (11.4%), and A3 (10.0%). The A4 (Asian) sublineage had a higher risk of CIN2+ than the A1–3 (European) sublineages (OR = 2.69, 95% CI = 1.04–6.97, P < 0.05). Furthermore, nucleotide variation in HPV16 E6 T178G is associated with the development of cervical cancer. Conclusion These data could provide novel insights into the role of HPV16 variants in cervical carcinogenesis risk in China.


2006 ◽  
Vol 319 (1) ◽  
pp. 488-496 ◽  
Author(s):  
Piyush M. Vyas ◽  
Sanjoy Roychowdhury ◽  
Farah D. Khan ◽  
Thomas E. Prisinzano ◽  
Jatinder Lamba ◽  
...  

Oncogene ◽  
2016 ◽  
Vol 36 (7) ◽  
pp. 956-965 ◽  
Author(s):  
R Molinuevo ◽  
A Freije ◽  
I de Pedro ◽  
S W Stoll ◽  
J T Elder ◽  
...  

2020 ◽  
Vol 34 (10) ◽  
pp. 13211-13223
Author(s):  
Rongying Ou ◽  
Mingfen Lv ◽  
Xuan Liu ◽  
Jiangmin Lv ◽  
Jinduo Zhao ◽  
...  

2000 ◽  
Vol 278 (4) ◽  
pp. C822-C833 ◽  
Author(s):  
Krystyna E. Rys-Sikora ◽  
Raymond L. Konger ◽  
John W. Schoggins ◽  
Rama Malaviya ◽  
Alice P. Pentland

PGE2 levels are altered in human epidermis after in vivo wounding; however, mechanisms modulating PGE2 production in activated keratinocytes are unclear. In previous studies, we showed that PGE2 is a growth-promoting autacoid in human primary keratinocyte cultures, and its production is modulated by plating density, suggesting that regulated PGE2 synthesis is an important component of wound healing. Here, we examine the role of phospholipase A2(PLA2) and cyclooxygenase (COX) enzymes in modulation of PGE2 production. We report that the increased PGE2 production that occurs in keratinocytes grown in nonconfluent conditions is also observed after in vitro wounding, indicating that similar mechanisms are involved. This increase was associated with coordinate upregulation of both COX-2 and secretory PLA2 (sPLA2) proteins. Increased sPLA2 activity was also observed. By RT-PCR, we identified the presence of type IIA and type V sPLA2, along with the M-type sPLA2 receptor. Thus the coordinate expression of sPLA2 and COX-2 may be responsible for the increased prostaglandin synthesis in activated keratinocytes during wound repair.


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