scholarly journals The role of gC1qR in regulating survival of human papillomavirus 16 oncogene-transfected cervical cancer cells

2011 ◽  
Author(s):  
Yu-Zhu Peng
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Human Papillomavirus 16 ◽  
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

MiR-34a Inhibits Viability and Invasion of Human Papillomavirus–Positive Cervical Cancer Cells by Targeting E2F3 and Regulating Survivin

2015 ◽  
Vol 25 (4) ◽  
pp. 707-713 ◽  
Author(s):  
Dianzhong Geng ◽  
Xiaohua Song ◽  
Fangling Ning ◽  
Qianhua Song ◽  
Honghua Yin
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cell Viability ◽  
Cancer Cells ◽  
Survivin Expression ◽  
Hpv Infection ◽  
Cervical Cancer Cells ◽  
Direct Target ◽  
Human Papillomavirus 18

ObjectivePrevious studies confirmed that high-risk human papillomavirus (HR-HPV) infection is a risk factor of cervical cancer, and the infection was associated with significantly reduced miR-34a expression during carcinogenesis. However, the downstream targets of miR-34a and their roles are still not well understood. This study explored the regulative role of miR-34a on E2F3 and survivin expression and the viability and invasion of HPV-positive cervical cancer cells.MethodsMiR-34a and survivin expression in 56 cases of HR-HPV–positive patients, 28 cases of HR-HPV–negative patients, and 28 normal cases without HR-HPV infections were measured. Human papillomavirus-18–positive HeLa cervical cancer cells and HPV-16–positive SiHa cells were used to explore the effect of miR-34a on cell viability and invasion. The molecular target of miR-34a was also explored in cervical cancer cells.ResultsThe results showed that miR-34a overexpression could inhibit HPV-positive cancer cell viability, whereas its downregulation promoted cell viability. E2F3 is a direct target of miR-34a in HPV-positive cervical cancer cells. By targeting E2F3, miR-34a could regulate the expression of survivin. Thus, through regulating E2F3 and survivin, miR-34a could reduce the viability and invasion of HPV-positive cervical cancer cells.ConclusionsThis study confirmed a novel miR-34a–E2F3–survivin axis in the tumor suppressor role of miR-34a in cervical cancer.

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
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