scholarly journals Adenovirus-Mediated p21(WAF1/SDII/CIP1)Gene Transfer Induces Apoptosis of Human Cervical Cancer Cell Lines

1999 ◽  
Vol 73 (6) ◽  
pp. 4983-4990 ◽  
Author(s):  
Yeou-Ping Tsao ◽  
Shyh-Jer Huang ◽  
Junn-Liang Chang ◽  
Jer-Tsong Hsieh ◽  
Rey-Chen Pong ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
High Efficiency ◽  
Recombinant Adenovirus ◽  
Chromatin Condensation ◽  
Adenovirus Vector ◽  
Cervical Cancer Cells ◽  
Apoptotic Effect ◽  
Human Cervical Cancer

ABSTRACT p21(WAF1/SDII/CIP1) (p21) arrests cell growth by inhibiting cyclin-depend kinases. To explore the potential of using p21 for the gene therapy of cervical cancer, we infected human papillomavirus (HPV)-positive cervical cancer cells (HeLa, SiHa, and Z172) and HPV-negative cervical cancer cells (C33A) with recombinant adenovirus encoding p21 cDNA. The results revealed that effective inhibition of cell growth could be achieved by sense p21 adenovirus but not antisense p21 adenovirus infection and occurred through apoptosis as measured by DNA fragmentation and chromatin condensation. Apoptosis was also observed in xenografts of human cervical cancer cells infected with sense p21 adenovirus, as confirmed by in situ terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL). The apoptosis was not prevented by overexpression of the bcl-2 transgene. To sum up, the apoptotic effect suggests that p21 should be a tumoricidal agent instead of a tumoristatic agent in preventing cervical cancers. In addition, our report substantiates the combination of the high efficiency of adenovirus vector-mediated gene delivery and the apoptotic effect of p21.

scholarly journals Upregulation of miR-205 induces CHN1 expression, which is associated with the aggressive behaviour of cervical cancer cells and correlated with lymph node metastasis

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jianbing Liu ◽  
Yunfeng Li ◽  
Xihua Chen ◽  
Xiangbo Xu ◽  
Haoqi Zhao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Lymph Node ◽  
High Risk ◽  
Cell Growth ◽  
Lymph Node Metastasis ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer

Abstract Background Cervical cancer is the leading cause of cancer-related death in women worldwide. However, the mechanisms mediating the development and progression of cervical cancer are unclear. In this study, we aimed to elucidate the roles of microRNAs and a1-chimaerin (CHN1) protein in cervical cancer progression. Methods The expression of miR-205 and CHN1 protein was investigated by in situ hybridisation and immunohistochemistry. We predicted the target genes of miR-205 using software prediction and dual luciferase assays. The expression of mRNAs and proteins was tested by qRT-PCR and western blotting respectively. The ability of cell growth, migration and invasion was evaluated by CCK-8 and transwell. Cell apoptosis was analysed by flow cytometry analysis. Results We found that miR-205 and CHN1 were highly expressed in human cervical cancer tissue compared with paired normal cervical tissues. The CHN1 gene was shown to be targeted by miR-205 in HeLa cells. Interestingly, transfection with miR-205 mimic upregulated CHN1 mRNA and protein, while miR-205 inhibitor downregulated CHN1 in high-risk and human papilloma virus (HPV)-negative human cervical cancer cells in vitro,. These data suggested that miR-205 positively regulated the expression of CHN1. Furthermore, the miR-205 mimic promoted cell growth, apoptosis, migration, and invasion in high-risk and HPV-negative cervical cancer cells, while the miR-205 inhibitor blocked these biological processes. Knockdown of CHN1 obviously reduced the aggressive cellular behaviours induced by upregulation of miR-205, suggesting that miR-205 positively regulated CHN1 to mediate these cell behaviours during the development of cervical cancer. Furthermore, CHN1 was correlated with lymph node metastasis in clinical specimens. Conclusions Our findings showed that miR-205 positively regulated CHN1 to mediate cell growth, apoptosis, migration, and invasion during cervical cancer development, particularly for high-risk HPV-type cervical cancer. These findings suggested that dysregulation of miR-205 and subsequent abnormalities in CHN1 expression promoted the oncogenic potential of 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.

scholarly journals Upregulation of miR-205 induces CHN1 expression, which is associated with the aggressive behaviour of cervical cancer cells and correlated with lymph node metastasis

2020 ◽  
Author(s):  
jianbing liu ◽  
yunfeng li ◽  
xihua chen ◽  
xiangbo xu ◽  
haoqi zhao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Lymph Node ◽  
High Risk ◽  
Cell Growth ◽  
Lymph Node Metastasis ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer

Abstract Background: Cervical cancer is the leading cause of cancer-related death in women worldwide. However, the mechanisms mediating the development and progression of cervical cancer are unclear. In this study, we aimed to elucidate the roles of microRNAs and a1-chimaerin (CHN1) protein in cervical cancer progression. Methods: The expression of miR-205 and CHN1 protein was investigated by in situ hybridisation and immunohistochemistry. We predicted the target genes of miR-205 using software prediction and dual luciferase assays. The expression of mRNAs and proteins was tested by qRT-PCR and western blotting respectively. The ability of cell growth, migration and invasion was evaluated by CCK-8 and transwell. Cell apoptosis was analysed by flow cytometry analysis. Results: We found that miR-205 and CHN1 were highly expressed in human cervical cancer tissue compared with paired normal cervical tissues. The CHN1 gene was shown to be targeted by miR-205 in HeLa cells. Interestingly, transfection with miR-205 mimic upregulated CHN1 mRNA and protein, while miR-205 inhibitor downregulated CHN1 in high-risk and human papilloma virus (HPV)-negative human cervical cancer cells in vitro ,. These data suggested that miR-205 positively regulated the expression of CHN1. Furthermore, the miR-205 mimic promoted cell growth, apoptosis, migration, and invasion in high-risk and HPV-negative cervical cancer cells, while the miR-205 inhibitor blocked these biological processes. Knockdown of CHN1 obviously reduced the aggressive cellular behaviours induced by upregulation of miR-205 , suggesting that miR-205 positively regulated CHN1 to mediate these cell behaviours during the development of cervical cancer. Furthermore, CHN1 was correlated with lymph node metastasis in clinical specimens. Conclusions: Our findings showed that miR-205 positively regulated CHN1 to mediate cell growth, apoptosis, migration, and invasion during cervical cancer development, particularly for high-risk HPV-type cervical cancer. These findings suggested that dysregulation of miR-205 and subsequent abnormalities in CHN1 expression promoted the oncogenic potential of human cervical cancer .

scholarly journals Upregulation of miR-205 induces CHN1 expression, which is associated with the aggressive behaviour of cervical cancer cells and correlated with lymph node metastasis

2019 ◽  
Author(s):  
jianbing liu ◽  
yunfeng li ◽  
xihua chen ◽  
xiangbo xu ◽  
haoqi zhao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Lymph Node ◽  
High Risk ◽  
Cell Growth ◽  
Lymph Node Metastasis ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer

Abstract Cervical cancer is the leading cause of cancer-related death in women worldwide. However, the mechanisms mediating the development and progression of cervical cancer are unclear. In this study, we aimed to elucidate the roles of microRNAs and CHN1 protein in cervical cancer progression. We found that miR-205 and CHN1 were highly expressed in human cervical cancer tissue compared with paired normal cervical tissues. The CHN1 gene was shown to be targeted by miR-205 in HeLa cells using software prediction and dual luciferase assays. Interestingly, transfection with miR-205 mimic upregulated CHN1 mRNA and protein, while miR-205 inhibitor downregulated CHN1 in high-risk and human papilloma virus (HPV)-negative human cervical cancer cells in vitro, as demonstrated by qRT-PCR and western blotting. These data suggested that miR-205 positively regulated the expression of CHN1. Furthermore, the miR-205 mimic promoted cell growth, apoptosis, migration, and invasion in high-risk and HPV-negative cervical cancer cells, while the miR-205 inhibitor blocked these biological processes. Knockdown of CHN1 obviously reduced the aggressive cellular behaviours induced by upregulation of miR-205, suggesting that miR-205 positively regulated CHN1 to mediate these cell behaviours during the development of cervical cancer. Furthermore, CHN1 was correlated with lymph node metastasis in clinical specimens, as shown by immunohistochemistry. Taken together, our findings showed that miR-205 positively regulated CHN1 to mediate cell growth, apoptosis, migration, and invasion during cervix cancer development, particularly for high-risk HPV-type cervical cancer. These findings suggested that dysregulation of miR-205 and subsequent abnormalities in CHN1 expression promoted the oncogenic potential of human cervical cancer.

scholarly journals Trifluoromethyl-phenyl-triazolyl derivative of beta-bisabolol induces cell death in ME-180 cervical cancer cells through induction of apoptosis and ROS generation

2015 ◽  
Vol 11 (1) ◽  
pp. 43
Author(s):  
Shu-Hong Hu ◽  
Hui Yu ◽  
Xue-Qin Gong ◽  
Ying-Hong Zhang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Phase Contrast ◽  
Chromatin Condensation ◽  
Flow Cytometric Analysis ◽  
Ros Generation ◽  
Dependent Manner ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

<p class="Abstract">The aim of the current investigation was to design, synthesize and demonstrate the anticancer and apoptotic activity of trifluoromethyl-phenyl-triazolyl derivative of beta-bisabolol (TTB) in ME-180 human cervical cancer cells.  MTT and clonogenic assays were used to evaluate the cell viability and colony formation tendencies of the cells respectively. Phase contrast and fluorescence microscopic investigations were used to evaluate the effect of TTB on cellular morphology and apoptosis. Flow cytometric analysis using fluorescent CM-DCFH2-DA were used to study the effect of TTB on reactive oxygen species (ROS) formation. The results revealed that TTB significantly inhibited the proliferation of ME-180 human cervical cancer cells in a time-dependent as well as dose-dependent manner. TTB has the capacity to inhibit both anchorage dependent as well as anchorage independent growth of ME-180 cervical cancer cells. TTB-treated cells revealed chromatin condensation, fragmented nuclei and nuclear shrinkage. A 3-fold increase of ROS production was seen after 72 μM TTB treatment.</p><p><strong><br /></strong></p><p><strong>VIDEO CLIPS</strong></p><p><a href="https://www.youtube.com/v/9yrPL3uy6Ls">Phase contrast microscopic study:</a>  2 min</p><p> </p>

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