scholarly journals Tobacco Exposure Enhances Human Papillomavirus 16 Oncogene Expression via EGFR/PI3K/Akt/c-Jun Signaling Pathway in Cervical Cancer Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Juan P. Muñoz ◽  
Diego Carrillo-Beltrán ◽  
Víctor Aedo-Aguilera ◽  
Gloria M. Calaf ◽  
Oscar León ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Tobacco Exposure ◽  
Human Papillomavirus 16 ◽  
Oncogene Expression ◽  
Cervical Cancer Cells

scholarly journals Leukemia Inhibitory Factor Downregulates Human Papillomavirus-16 Oncogene Expression and Inhibits the Proliferation of Cervical Carcinoma Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Joseph M. Bay ◽  
Bruce K. Patterson ◽  
Nelson N. H. Teng
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Leukemia Inhibitory Factor ◽  
Inhibitory Factor ◽  
Human Papillomavirus 16 ◽  
Oncogene Expression ◽  
Hpv E6 ◽  
Cervical Cancer Cells ◽  
E6 And E7

The constitutive proliferation and resistance to differentiation and apoptosis of neoplastic cervical cells depend on sustained expression of human papillomavirus oncogenes. Inhibition of these oncogenes is a goal for the prevention of progression of HPV-induced neoplasias to cervical cancer. SiHa cervical cancer cells were transfected with an HPV-16 promoter reporter construct and treated with leukemia inhibitory factor (LIF), a human cytokine of the interleukin 6 superfamily. SiHa and CaSki cervical cancer cells were also assessed for proliferation by MTT precipitation, programmed cell death by flow cytometry, and HPV E6 and E7 expression by real-time PCR. LIF-treated cervical cancer cells showed significantly reduced HPV LCR activation, reduced levels of E6 and E7 mRNA, and reduced proliferation. We report the novel use of LIF to inhibit viral oncogene expression in cervical cancer cells, with concomitant reduction in proliferation suggesting re-engagement of cell-cycle regulation.

scholarly journals In vitro and in vivo growth suppression of human papillomavirus 16-positive cervical cancer cells by e6 siRNA

2003 ◽  
Vol 8 (5) ◽  
pp. 762-768 ◽  
Author(s):  
Mitsuo Yoshinouchi ◽  
Taketo Yamada ◽  
Masahiro Kizaki ◽  
Jin Fen ◽  
Takeyoshi Koseki ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Growth Suppression ◽  
Human Papillomavirus 16 ◽  
Cervical Cancer Cells ◽  
In Vivo Growth

Human papillomavirus 16 E6, E7 siRNAs inhibit proliferation and induce apoptosis of SiHa cervical cancer cells

2008 ◽  
Vol 20 (4) ◽  
pp. 301-306 ◽  
Author(s):  
Chun-lian Nie ◽  
Guo-lan Gao ◽  
Jie Han ◽  
Hua Li ◽  
He-ping Chen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Human Papillomavirus 16 ◽  
Cervical Cancer Cells

scholarly journals Plasma-based Endogenous Metabolomics Profiling of High-Risk Human Papillomavirus and Their Emerging Roles in the Progression of Cervical Cancer

2021 ◽  
Author(s):  
Qin Wang ◽  
Min Xu ◽  
Tingting Chen ◽  
Jing Chen ◽  
Runjie Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
High Risk ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Metabolic Phenotype ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract Objective: High-risk human papillomavirus (HR-HPV) is the main etiological factor for cervical cancer. Accumulating evidence has suggested that the active role of metabolites in the initiation and progression of cancers. This study was to explore the metabolic profiles of HR-HPV infection and their potential functions in cervical cancer.Methods: Non-targeted metabolomics approach was used to detect metabolic alterations in the plasma obtained from HPV-16 positive (HPV16 (+)), HPV-18 positive (HPV18 (+)) and HPV negative (CTL) individuals, followed by CCK8 experiment to detect the effect of different metabolites on the proliferation of Hela and GH354. A cell migration test then verified significant metabolites on the migration of Hela and GH354. Q RT-qPCR and western blot were used to detect malignant progression related mRNA and protein expression levels of cervical cancer.Results: HR-HPV groups shared 24 dysregulated metabolites (such as amino acids, ceramides, glycerophosphocholines). Further experiments showed ceramide species, including C8 inhibits cervical cancer cells proliferation and migration in vitro. In contrast, C12 significantly enhanced cervical cancer cells proliferation and migration in vitro. Protein and mRNA expressions indicated C8 and C12 were related to the malignant behavior of cervical cancer in vitro. The underlying mechanism demonstrated that C8 intervention inhibited proliferation and migration in cervical cancer cells via the MAPK/JNK signaling pathway, while C12 intervention promoted proliferation and migration in cervical cancer cells via the MAPK/ERK signaling pathway. These findings may contribute to the treatment of HR-HPV-induced cervical cancer by intervening in its initiation and progression.Conclusion: Our study shed some light on how metabolites influenced the relationship between HR-HPV oncogenic capability and metabolic phenotype change and identify species C8 and C12 as critical lipid metabolites that modulate cervical cancer cell’s function.

scholarly journals Long non-coding RNA FAM83H-AS1 is regulated by human papillomavirus 16 E6 independently of p53 in cervical cancer cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jamie A. Barr ◽  
Karen E. Hayes ◽  
Tayvia Brownmiller ◽  
Abby D. Harold ◽  
Rajaganapathi Jagannathan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Human Papillomavirus 16 ◽  
Non Coding Rna ◽  
Cervical Cancer Cells ◽  
Long Non Coding Rna
Sign in / Sign up

Export Citation Format

Share Document