Down-regulation of phospho-non-receptor Src tyrosine kinases contributes to growth inhibition of cervical cancer cells

2010 ◽  
Vol 28 (4) ◽  
pp. 1495-1506 ◽  
Author(s):  
Lu Kong ◽  
Zhihong Deng ◽  
Yanzhong Zhao ◽  
Yamei Wang ◽  
Fazlul H. Sarkar ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Tyrosine Kinases ◽  
Down Regulation ◽  
Src Tyrosine Kinases ◽  
Cervical Cancer Cells

scholarly journals Retraction: Down-regulation of the radiation-induced pEGFRThr654 mediated activation of DNA-PK by Cetuximab in cervical cancer cells

RSC Advances ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 5021-5021
Author(s):  
Laura Fisher
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Down Regulation ◽  
Cervical Cancer Cells ◽  
Radiation Induced

Retraction of ‘Down-regulation of the radiation-induced pEGFRThr654 mediated activation of DNA-PK by Cetuximab in cervical cancer cells’ by Yunxiang Qi et al., RSC Adv., 2020, 10, 1132–1141, DOI: 10.1039/C9RA04962B.

Silencing of HPV 18 Oncoproteins With RNA Interference Causes Growth Inhibition of Cervical Cancer Cells

2007 ◽  
Vol 14 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Jayanthi S. Lea ◽  
Noriaki Sunaga ◽  
Mitsuo Sato ◽  
Geetha Kalahasti ◽  
David S. Miller ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Rna Interference ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Hpv 18

Growth Inhibition of Human Cervical Cancer Cells with the Recombinant Adenovirusp53 in Vitro

1996 ◽  
Vol 60 (3) ◽  
pp. 373-379 ◽  
Author(s):  
Katsuyuki Hamada ◽  
Wei-Wei Zhang ◽  
Ramon Alemany ◽  
Judith Wolf ◽  
Jack A. Roth ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

scholarly journals Disruption of HPV16-E7 by CRISPR/Cas System Induces Apoptosis and Growth Inhibition in HPV16 Positive Human Cervical Cancer Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Zheng Hu ◽  
Lan Yu ◽  
Da Zhu ◽  
Wencheng Ding ◽  
Xiaoli Wang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Hpv Infection ◽  
Hek293 Cells ◽  
Guide Rna ◽  
System A ◽  
Cervical Cancer Cells ◽  
E6 And E7 ◽  
Human Cervical Cancer Cells

High-risk human papillomavirus (HR-HPV) has been recognized as a major causative agent for cervical cancer. Upon HPV infection, early genes E6 and E7 play important roles in maintaining malignant phenotype of cervical cancer cells. By using clustered regularly interspaced short palindromic repeats- (CRISPR-) associated protein system (CRISPR/Cas system), a widely used genome editing tool in many organisms, to target HPV16-E7 DNA in HPV positive cell lines, we showed for the first time that the HPV16-E7 single-guide RNA (sgRNA) guided CRISPR/Cas system could disrupt HPV16-E7 DNA at specific sites, inducing apoptosis and growth inhibition in HPV positive SiHa and Caski cells, but not in HPV negative C33A and HEK293 cells. Moreover, disruption of E7 DNA directly leads to downregulation of E7 protein and upregulation of tumor suppressor protein pRb. Therefore, our results suggest that HPV16-E7 gRNA guided CRISPR/Cas system might be used as a therapeutic strategy for the treatment of cervical cancer.

Notch1 induces cell cycle arrest and apoptosis in human cervical cancer cells: involvement of nuclear factor kappa B inhibition

2007 ◽  
Vol 17 (2) ◽  
pp. 502-510 ◽  
Author(s):  
J. Yao ◽  
L. Duan ◽  
M. Fan ◽  
J. Yuan ◽  
X. Wu
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Cycle Arrest ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Notch signaling can serve as a tumor suppressor or tumor promoter in the same kind of cancer, such as human papillomavirus–positive cervical cancer cells. However, the exact mechanisms remain poorly characterized. Our studies demonstrated that constitutively overexpressed active Notch1 via stable transfection with exogenous intracellular domain of Notch1 (ICN) resulted in growth inhibition of the human cervical cancer cell line HeLa by inducing G2–M arrest and apoptosis. Moreover, the growth inhibition was correlated with inhibition of nuclear factor kappa B (NF-κB) p50 activation, accompanied by a decrease in the nuclear expression of NF-κB p50 and an increase in the cytosolic expression of IκBα. Consistent with these results, downregulation of cyclin D1 and Bcl-2, which are both the downstream genes of NF-κB, were observed in ICN-overexpressed cells. Overall, our results suggest that NF-κB inhibition may contribute partially to cell cycle arrest and apoptosis induced by Notch1 activation in human cervical cancer cells.

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