scholarly journals Thymoquinone Inhibits the Migration and Invasive Characteristics of Cervical Cancer Cells SiHa and CaSki In Vitro by Targeting Epithelial to Mesenchymal Transition Associated Transcription Factors Twist1 and Zeb1

Molecules ◽  
2017 ◽  
Vol 22 (12) ◽  
pp. 2105 ◽  
Author(s):  
Jun Li ◽  
Md. Khan ◽  
Chunli Wei ◽  
Jingliang Cheng ◽  
Hanchun Chen ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Cervical Cancer Cells

scholarly journals CD36 promotes the epithelial–mesenchymal transition and metastasis in cervical cancer by interacting with TGF-β

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Min Deng ◽  
Xiaodong Cai ◽  
Ling Long ◽  
Linying Xie ◽  
Hongmei Ma ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Cd36 Expression ◽  
Cervical Cancer Cells

Abstract Background Accumulating evidence indicates that CD36 initiates metastasis and correlates with an unfavorable prognosis in cancers. However, there are few reports regarding the roles of CD36 in initiation and metastasis of cervical cancer. Methods Using immunohistochemistry, we analyzed 133 cervical cancer samples for CD36 protein expression levels, and then investigated the correlation between changes in its expression and clinicopathologic parameters. The effect of CD36 expression on the epithelial–mesenchymal transition (EMT) in cervical cancer cells was evaluated by Western immunoblotting analysis. In vitro invasion and in vivo metastasis assays were also used to evaluate the role of CD36 in cervical cancer metastasis. Results In the present study, we confirmed that CD36 was highly expressed in cervical cancer samples relative to normal cervical tissues. Moreover, overexpression of CD36 promoted invasiveness and metastasis of cervical cancer cells in vitro and in vivo, while CD36 knockdown suppressed proliferation, migration, and invasiveness. We demonstrated that TGF-β treatment attenuated E-cadherin expression and enhanced the expression levels of CD36, vimentin, slug, snail, and twist in si-SiHa, si-HeLa, and C33a–CD36 cells, suggesting that TGF-β synergized with CD36 on EMT via active CD36 expression. We also observed that the expression levels of TGF-β in si-SiHa cells and si-HeLa cells were down-regulated, whereas the expression levels of TGF-β were up-regulated in C33a–CD36 cells. These results imply that CD36 and TGF-β interact with each other to promote the EMT in cervical cancer. Conclusions Our findings suggest that CD36 is likely to be an effective target for guiding individualized clinical therapy of cervical cancer.

hCINAP is a potential direct HIF-1 target gene and is required for hypoxia-induced EMT and apoptosis in cervical cancer cells

2020 ◽  
Author(s):  
yong zhang ◽  
li jiang ◽  
nianqun qin ◽  
Mi Cao ◽  
xiujuan Liang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Target Gene ◽  
Epithelial To Mesenchymal Transition ◽  
Critical Role ◽  
Surrounding Tissue ◽  
Mesenchymal Transition ◽  
Migratory Capacity ◽  
Signal Input ◽  
Cervical Cancer Cells

The early metastasis of cervical cancer is a multi-step process requiring the cancer cells to adapt to the signal input from different tissue environments, including hypoxia. Hypoxia-induced epithelial-to-mesenchymal transition (EMT) plays a critical role in the acquisition of the ability to invade surrounding tissue. However, the molecular mechanism underlying EMT in cervical cancer remains to be elucidated. Herein, we showed that HIF‑1α and ARNT are recruited to the hCINAP promoter and initiate hCINAP expression in hypoxia. Ablation of hCINAP decreased the migratory capacity and EMT of cervical cancer cells in hypoxia. Furthermore, hCINAP regulates EMT through Akt/mTOR signaling and inhibits hypoxia-induced p53-dependent apoptosis. Our data collectively showed that hCINAP may have essential roles in the metastasis of cervical cancer and could be a potential target for curing cervical cancer.

scholarly journals Bazedoxifene, a GP130 Inhibitor, Modulates EMT Signaling and Exhibits Antitumor Effects in HPV-Positive Cervical Cancer

2021 ◽  
Vol 22 (16) ◽  
pp. 8693
Author(s):  
Leekyung Kim ◽  
Sun-Ae Park ◽  
Hyemin Park ◽  
Heejung Kim ◽  
Tae-Hwe Heo
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Drug Repositioning ◽  
Antitumor Effects ◽  
Mesenchymal Transition ◽  
Stat3 Pathway ◽  
Cervical Cancer Cells

Persistent HPV (Human Papillomavirus) infection is the primary cause of cervical cancer. Despite the development of the HPV vaccine to prevent infections, cervical cancer is still a fatal malignant tumor and metastatic disease, and it is often difficult to treat, so a new treatment strategy is needed. The FDA-approved drug Bazedoxifene is a novel inhibitor of protein–protein interactions between IL-6 and GP130. Multiple ligand simultaneous docking and drug repositioning approaches have demonstrated that an IL-6/GP130 inhibitor can act as a selective estrogen modulator. However, the molecular basis for GP130 activation in cervical cancer remains unclear. In this study, we investigated the anticancer properties of Bazedoxifene in HPV-positive cervical cancer cells. In vitro and in vivo experiments showed that Bazedoxifene inhibited cell invasion, migration, colony formation, and tumor growth in cervical cancer cells. We also confirmed that Bazedoxifene inhibits the GP130/STAT3 pathway and suppresses the EMT (Epithelial-mesenchymal transition) sub-signal. Thus, these data not only suggest a molecular mechanism by which the GP130/STAT3 pathway may promote cancer, but also may provide a basis for cervical cancer replacement therapy.

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