scholarly journals Long (27-nucleotides) small inhibitory RNAs targeting E6 protein eradicate effectively the cervical cancer cells harboring human papilloma virus

2015 ◽  
Vol 58 (3) ◽  
pp. 210 ◽  
Author(s):  
Jun Sik Cho ◽  
Shin-Wha Lee ◽  
Yong-Man Kim ◽  
Dongho Kim ◽  
Dae-Yeon Kim ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papilloma Virus ◽  
Cancer Cells ◽  
Papilloma Virus ◽  
Cervical Cancer Cells ◽  
E6 Protein

scholarly journals Extracellular Vesicles from Human Papilloma Virus-Infected Cervical Cancer Cells Enhance HIV-1 Replication in Differentiated U1 Cell Line

Viruses ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 239 ◽  
Author(s):  
Sabina Ranjit ◽  
Sunitha Kodidela ◽  
Namita Sinha ◽  
Subhash Chauhan ◽  
Santosh Kumar
Keyword(s):  
Oxidative Stress ◽  
Cervical Cancer ◽  
Human Papilloma Virus ◽  
Cancer Cells ◽  
Cell Line ◽  
Extracellular Vesicles ◽  
Papilloma Virus ◽  
Cervical Cancer Cells ◽  
Hpv Oncoproteins ◽  
Hiv 1

In the current study, we hypothesized that extracellular vesicles (EVs) secreted from human papilloma virus (HPV)-infected cervical cancer cells exacerbate human immunodeficiency virus (HIV)-1 replication in differentiated U1 cell line through an oxidative stress pathway. To test the hypothesis, we treated an HIV-1-infected macrophage cell line (U1) with HPV-infected Caski cell culture supernatant (CCS). We observed a significant increase in HIV-1 replication, which was associated with an increase in the expression of cytochrome P450 (CYPs 1A1 and 2A6) in the CCS-treated U1 cells. Furthermore, we isolated EVs from CCS (CCS-EVs), which showed the presence of CYPs (1A1, 2A6), superoxide dismutase 1 (SOD1), and HPV oncoproteins HPV16 E6. CCS-EVs when exposed to the U1 cells also significantly increased HIV-1 replication. Treatment of antioxidant, CYP1A1 and CYP2A6 inhibitors, and chemodietary agents with antioxidant properties significantly reduced the CCS and CCS-EVs mediated HIV-1 replication in U1 cells. Altogether, we demonstrate that cervical cancer cells exacerbate HIV-1 replication in differentiated U1 cell line via transferring CYPs and HPV oncoproteins through EVs. We also show that the viral replication occurs via CYP and oxidative stress pathways, and the viral replication is also reduced by chemodietary agents. This study provides important information regarding biological interactions between HPV and HIV-1 via EVs leading to enhanced HIV-1 replication.

scholarly journals Endogenous Human Papillomavirus E6 and E7 Proteins Differentially Regulate Proliferation, Senescence, and Apoptosis in HeLa Cervical Carcinoma Cells

2003 ◽  
Vol 77 (2) ◽  
pp. 1551-1563 ◽  
Author(s):  
Rosa Anna DeFilippis ◽  
Edward C. Goodwin ◽  
Lingling Wu ◽  
Daniel DiMaio
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Cervical Carcinoma ◽  
Carcinoma Cells ◽  
Rb Pathway ◽  
Cervical Cancer Cells ◽  
E6 And E7 ◽  
E7 Proteins ◽  
E6 Protein

ABSTRACT Cervical cancer cells express high-risk human papillomavirus (HPV) E6 and E7 proteins, and repression of HPV gene expression causes the cells to cease proliferation and undergo senescence. However, it is not known whether both HPV proteins are required to maintain the proliferative state of cervical cancer cells, or whether mutations that accumulate during carcinogenesis eliminate the need for one or the other of them. To address these questions, we used the bovine papillomavirus E2 protein to repress the expression of either the E6 protein or the E7 protein encoded by integrated HPV18 DNA in HeLa cervical carcinoma cells. Repression of the E7 protein activated the Rb pathway but not the p53 pathway and triggered senescence, whereas repression of the E6 protein activated the p53 pathway but not the Rb pathway and triggered both senescence and apoptosis. Telomerase activity, cyclin-dependent kinase activity, and expression of c-myc were markedly inhibited by repression of either E6 or E7. These results demonstrate that continuous expression of both the E6 and the E7 protein is required for optimal proliferation of cervical carcinoma cells and that the two viral proteins exert distinct effects on cell survival and proliferation. Therefore, strategies that inhibit the expression or activity of either viral protein are likely to inhibit the growth of HPV-associated cancers.

CD71+ Population Enriched by HPV-E6 Protein Promotes Cancer Aggressiveness and Radioresistance in Cervical Cancer Cells

2019 ◽  
Vol 17 (9) ◽  
pp. 1867-1880 ◽  
Author(s):  
Thomas Ho-Yin Leung ◽  
Hermit Wai-Man Tang ◽  
Michelle Kwan-Yee Siu ◽  
David Wai Chan ◽  
Karen Kar-Loen Chan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Hpv E6 ◽  
Cancer Aggressiveness ◽  
Cervical Cancer Cells ◽  
E6 Protein

scholarly journals A BRIEF REVIEW ON CRYOGUN MACHINE FOR PRE-CERVIX CANCER HEALING

2021 ◽  
Vol 3 (1) ◽  
pp. 32
Author(s):  
Aji Bagaskara ◽  
Rita Sundari ◽  
Rini Anggraini
Keyword(s):  
Cervical Cancer ◽  
Virus Infection ◽  
Human Papilloma Virus ◽  
Cancer Cells ◽  
Cervix Cancer ◽  
Papilloma Virus ◽  
Ablation Therapy ◽  
Cone Biopsy ◽  
Cancer Diseases

 Cervical cancer is generally found in women of all ages due to  virus infection on epithelial cells of female cervix. It is known that a certain type of Human Papilloma Virus (HPV) is suspected to cause cervix cancer in women from various ethnics.   Several therapies have been used to cure cancer diseases like cone biopsy, laser treatment, electrosurgical excision, thermocoagulation, ablation therapy, and cryotherapy. This paper has highlighted on the role of cryogun machine applied in cryotherapy for pre-cervical cancer treatment in relation to freezing technique using liquid nitrogen to kill cancer cells on infectious area.   

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