English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

High-risk human papillomaviruses (HR-HPVs) are consistently associated withhuman cervical cancer Additionally, the early oncoproteins of HPVs E5, E6 andE7 are known to contribute to tumor progression. The role of E5 is still nebulous.In this study, we aimed to explore the mechanism of E5 action during the humancervical carcinogenesis process. We created four cell models overexpressing HPV16or HPV18 E5 (HPV16/18 E5) and investigated their ability to proliferate, alongwith their metastatic characteristics such as migration and invasion. The expressionof HPV16/18 E5 protein in various cell lines was analyzed by reverse transcriptase-polymerasechain reaction (RT-PCR). In addition, we compared the levels of phosphorylatedpaxillin as well as E-cadherin in cell models and controls by western blot analysis.Finally, we assessed the tumor growth rate of human cervical cancer cells overexpressingHPV16/18 E5 in vivo. We discovered that the expression of HPV16/18 E5 consistentlyincreased the malignant potential of various human cervical cancer cells comparedwith the primary counterparts. We demonstrated the involvement of HPV16/18 E5in proliferation, migration, invasion and regulation of the actin cytoskeletonin human cervical cancer cells. In particular we discovered that HPV16/18 E5 overexpressionin human cervical cancer cells correlated with higher levels of paxillin proteinsphosphorylated on tyrosine residues and with the downregulation of E-cadherin.Importantly, injection of HPV16/18 E5-overexpressing human cervical cancer cellsinto mice increased both HPV-and non-HPV-derived tumor growth. Collectively, ourdata indicate that HPV16/18 E5 influences progression of the human cervical cancermalignant phenotype. This study provides new insights into HPV16/18 E5 as a possibleagent that may have an impact on the therapeutic strategies targeting human cervicalcancer.

Human papillomavirus 16/18 E5 promotes cervical cancer cell proliferation, migration and invasion in vitro and accelerates tumor growth in vivo