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.

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 Adenosine uptake is the major effector of extracellular ATP toxicity in human cervical cancer cells

2014 ◽  
Vol 25 (19) ◽  
pp. 2905-2918 ◽  
Author(s):  
Paola de Andrade Mello ◽  
Eduardo Cremonese Filippi-Chiela ◽  
Jéssica Nascimento ◽  
Aline Beckenkamp ◽  
Danielle Bertodo Santana ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Purinergic Signaling ◽  
Hpv Infection ◽  
Extracellular Atp ◽  
Parp Cleavage ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

In cervical cancer, HPV infection and disruption of mechanisms involving cell growth, differentiation, and apoptosis are strictly linked with tumor progression and invasion. Tumor microenvironment is ATP and adenosine rich, suggesting a role for purinergic signaling in cancer cell growth and death. Here we investigate the effect of extracellular ATP on human cervical cancer cells. We find that extracellular ATP itself has a small cytotoxic effect, whereas adenosine formed from ATP degradation by ectonucleotidases is the main factor responsible for apoptosis induction. The level of P2×7 receptor seemed to define the main cytotoxic mechanism triggered by ATP, since ATP itself eliminated a small subpopulation of cells that express high P2×7 levels, probably through its activation. Corroborating these data, blockage or knockdown of P2×7 only slightly reduced ATP cytotoxicity. On the other hand, cell viability was almost totally recovered with dipyridamole, an adenosine transporter inhibitor. Moreover, ATP-induced apoptosis and signaling—p53 increase, AMPK activation, and PARP cleavage—as well as autophagy induction were also inhibited by dipyridamole. In addition, inhibition of adenosine conversion into AMP also blocked cell death, indicating that metabolization of intracellular adenosine originating from extracellular ATP is responsible for the main effects of the latter in human cervical cancer cells.

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.

scholarly journals Caffeic acid phenethyl ester induces E2F-1-mediated growth inhibition and cell-cycle arrest in human cervical cancer cells

FEBS Journal ◽  
2013 ◽  
Vol 280 (11) ◽  
pp. 2581-2593 ◽  
Author(s):  
Tzu-Hui Hsu ◽  
Chin-Chen Chu ◽  
Mei-Whey Hung ◽  
Hwei-Jen Lee ◽  
Hsien-Jun Hsu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Caffeic Acid Phenethyl Ester ◽  
Cycle Arrest ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Genistein Induces Alterations of Epigenetic Modulatory Signatures in Human Cervical Cancer Cells

2018 ◽  
Vol 18 (3) ◽  
pp. 412-421 ◽  
Author(s):  
Madhumitha Kedhari Sundaram ◽  
Mohammad Zeeshan Ansari ◽  
Abdullah Al Mutery ◽  
Maryam Ashraf ◽  
Reem Nasab ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
In Silico ◽  
Tumour Suppressor Genes ◽  
Dietary Polyphenols ◽  
In Silico Studies ◽  
Genistein Treatment ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

Introduction: Epidemiological studies indicate that diet rich in fruits and vegetables is associated with decreased cancer risk thereby indicating that dietary polyphenols can be potential chemo-preventive agents. The reversible nature of epigenetic modifications makes them a favorable target for cancer prevention. Polyphenols have been shown to reverse aberrant epigenetic patterns by targeting the regulatory enzymes, DNA methyltransferases (DNMTs) and histone deacetylases (HDACs). In vitro and in silico studies of DNMTs and HDACs were planned to examine genistein’s role as a natural epigenetic modifier in human cervical cancer cells, HeLa. Methods: Expression of the tumour suppressor genes (TSGs) [MGMT, RARβ, p21, E-cadherin, DAPK1] as well the methylation status of their promoters were examined alongwith the activity levels of DNMT and HDAC enzymes after treatment with genistein. Expression of DNMTs and HDACs was also studied. In-silico studies were performed to determine the interaction of genistein with DNMTs and HDACs. Results: Genistein treatment significantly reduced the expression and enzymatic activity of both DNMTs and HDACs in a time-dependent way. Molecular modeling data suggest that genistein can interact with various members of DNMT and HDAC families and support genistein mediated inhibition of their activity. Timedependent exposure of genistein reversed the promoter region methylation of the TSGs and re-established their expression. Conclusions: In this study, we find that genistein is able to reinstate the expression of the TSGs studied by inhibiting the action of DNMTs and HDACs. This shows that genistein could be an important arsenal in the development of epigenetic based cancer therapy.

scholarly journals Caffeic Acid Induces Apoptosis in Human Cervical Cancer Cells Through the Mitochondrial Pathway

2010 ◽  
Vol 49 (4) ◽  
pp. 419-424 ◽  
Author(s):  
Wei-Chun Chang ◽  
Ching-Hung Hsieh ◽  
Meen-Woon Hsiao ◽  
Wu-Chou Lin ◽  
Yao-Ching Hung ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Mitochondrial Pathway ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

scholarly journals Recombinant heat shock protein 27 (HSP27/HSPB1) protects against cadmium-induced oxidative stress and toxicity in human cervical cancer cells

2017 ◽  
Vol 22 (3) ◽  
pp. 357-369 ◽  
Author(s):  
Daiana G. Alvarez-Olmedo ◽  
Veronica S. Biaggio ◽  
Geremy A. Koumbadinga ◽  
Nidia N. Gómez ◽  
Chunhua Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cervical Cancer ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cancer Cells ◽  
Heat Shock Protein 27 ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer
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