Vitamin C Augments Chemotherapeutic Response of Cervical Carcinoma HeLa Cells by Stabilizing P53

2001 ◽  
Vol 282 (2) ◽  
pp. 409-415 ◽  
Author(s):  
Vijay G. Reddy ◽  
Neeru Khanna ◽  
Neeta Singh
2009 ◽  
Vol 76 (5) ◽  
pp. 998-1010 ◽  
Author(s):  
Sergio Anguissola ◽  
Barbara Köhler ◽  
Robert O'Byrne ◽  
Heiko Düssmann ◽  
Mary D. Cannon ◽  
...  

2016 ◽  
Vol 11 (4) ◽  
pp. 2440-2444 ◽  
Author(s):  
PING JIANG ◽  
YA-LI REN ◽  
JIA-LIANG LI ◽  
JUN LUO

2015 ◽  
Vol 24 (2) ◽  
pp. 665-672 ◽  
Author(s):  
Yu-Jin Hwang ◽  
Hae-Ri Wi ◽  
Haeng-Ran Kim ◽  
Kye Won Park ◽  
Kyung-A Hwang

2019 ◽  
Vol 25 (4) ◽  
pp. 217-223 ◽  
Author(s):  
Li-na Peng ◽  
Wen-tian Shi ◽  
Huan-rong Feng ◽  
Chuan-yu Wei ◽  
Qi-nan Yin

The aim of this study was to evaluate the effect of the miR-301a/PTEN pathway in cervical cancer. miR-301a and PTEN expression were measured by quantitative real-time PCR (qRT-PCR) in tissues samples and HeLa cells. PTEN protein level was determined by Western blotting. Dual reporter luciferase assay was performed to validate PTEN as a direct target of miR-301a. The gain- and loss-of function assay was performed by miR-301a overexpression and silencing. Cell proliferation was monitored by cell counting Kit-8 (CCK-8). Cell apoptosis was quantitated by flow cytometry. SPSS was used to analyze the significant difference in the treatments. miR-301a demonstrated a significantly higher expression in cervical carcinoma tissues compared with the paired non-carcinoma tissues ( n = 12), while PTEN expression was found to be significantly lower in cervical carcinoma tissues than their paired non-carcinoma tissues ( n = 12). In addition, PTEN was identified as the direct target of miR-301a. Moreover, overexpression of miR-301a significantly promoted HeLa cells proliferation and anti-apoptosis which had a reverse pattern after PTEN overexpression. Our results confirm PTEN as a direct target of miR-301a in HeLa cells and suggest that miR-301a/PTEN pathway contributes to the development and progression of cervical cancer.


Author(s):  
Robert Nawrot ◽  
Maria Wolun-Cholewa ◽  
Wojciech Bialas ◽  
Danuta Wyrzykowska ◽  
Stanislaw Balcerkiewicz ◽  
...  

2009 ◽  
Vol 87 (6) ◽  
pp. 933-942 ◽  
Author(s):  
Li Yang ◽  
Hai-wei Zhang ◽  
Rong Hu ◽  
Yong Yang ◽  
Qi Qi ◽  
...  

Wogonin, a naturally occurring flavonoid, has been shown to have tumor therapeutic potential both in vitro and in vivo. To better understand its anticancer mechanism, we examined the effect of wogonin on human cervical carcinoma HeLa cells. In this study, we observed that G1 phase arrest was involved in wogonin-induced growth inhibition in HeLa cells. Over a 24 h exposure of HeLa cells to 90 µmol·L–1 wogonin, the promoters of G1–S transition, including cyclin D1/Cdk4 and pRb, decreased within 12 h and E2F-1 depleted in the nucleus at the same time. As the G1 phase arrest developed, p53 and the Cdk inhibitor p21Cip1 elevated both at protein and mRNA levels. Furthermore, the up-regulation of p21Cip1 induced by wogonin was dramatically inhibited by siRNA-mediated p53 gene silencing. Collectively, our data suggested that wogonin induced G1 phase arrest in HeLa cells by modulating several key G1 regulatory proteins, such as Cdk4 and cyclin D1, as well as up-regulation of a p53-midiated p21Cip1 expression. This mechanism of wogonin may play an important role in the killing of cancerous cells and offer a potential mechanism for its anticancer action in vivo.


2012 ◽  
Vol 46 (9) ◽  
pp. 1082-1092 ◽  
Author(s):  
Simiao Fan ◽  
Yang Yu ◽  
Min Qi ◽  
Zhongdong Sun ◽  
Lihua Li ◽  
...  

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