scholarly journals Hypoxia and TGF-β1 induced PLOD2 expression improve the migration and invasion of cervical cancer cells by promoting epithelial-to-mesenchymal transition (EMT) and focal adhesion formation

2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Feifei Xu ◽  
Jialu Zhang ◽  
Guolin Hu ◽  
Lei Liu ◽  
Weijiang Liang
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Focal Adhesion ◽  
Epithelial To Mesenchymal Transition ◽  
Adhesion Formation ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Focal Adhesion Formation ◽  
Cervical Cancer Cells ◽  
Tgf Β1

The Impacts of Bone Marrow Mesenchymal Stem Cells (BMSCs)-Derived Periostin on Epithelial-Mesenchymal Transition (EMT) of Cervical Cancer Cells

2022 ◽  
Vol 12 (4) ◽  
pp. 820-826
Author(s):  
Chengyong Wu ◽  
Weifeng Wei ◽  
Jing Li ◽  
Shenglin Peng
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Signal Transduction Pathway ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Essential Components ◽  
Cervical Cancer Cells ◽  
E Cadherin

Epithelial-mesenchymal transition (EMT) is closely related to the migrating and invading behaviors of cells. Periostin is one of the essential components in the extracellular matrix and can induce EMT of cells and their sequential metastasis. But its underlying mechanism is unclear. The Hela and BMSC cell lines were assigned into Periostin-mimic group, Periostin-Inhibitor group and Periostin-NC group followed by analysis of cell migration and invasion, expression of E-Cadherin, Vimentin, β-Catenin, Snail, MMP-2, MMP-9, PTEN, and p-PTEN. Cells in Periostin-mimic group exhibited lowest migration, least number of invaded cells, as well as lowest levels of Vimentin, β-Catenin, Snail, MMP-2, MMP-9, p-PTEN, Akt, p-Akt, p-GSK-3β, p-PDK1 and p-cRcf, along with highest levels of E-cadherin and PTEN. Moreover, cells in Periostin-NC group had intermediate levels of these above indicators, while, the Periostin-Inhibitor group exhibited the highest migration rate, the most number of invaded cells, and the highest levels of these proteins (P < 0.05). In conclusion, BMSCs-derived Periostin can influence the EMT of cervical cancer cells possibly through restraining the activity of the PI3K/AKT signal transduction pathway, indicating that Periostin might be a target of chemotherapy in clinics for the treatment of cervical cancer.

scholarly journals Role of NAPDH oxidase and its therapeutic intervention in TGF-β-mediated EMT progression: an in vitro analysis on HeLa cervical cancer cells

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Karthika Muthuramalingam ◽  
Moonjae Cho ◽  
Youngmee Kim
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cellular Migration ◽  
Therapeutic Interventions ◽  
Migration And Invasion ◽  
Potent Inducer ◽  
Mesenchymal Transition ◽  
Redox Biology ◽  
Napdh Oxidase ◽  
Cervical Cancer Cells

AbstractEpithelial to mesenchymal transition (EMT) is a complex biological event, wherein polarized epithelial cells lose their integrity resulting in a mesenchymal phenotype with enhanced motility, a phenomenon known as metastasis. However, the underlying mechanisms of EMT are still poorly understood in cervical carcinomas. In this study, we investigated the molecular signalling events responsible for the effect of TGF-β, a potent inducer of EMT, on HeLa cervical cancer cells. We observed that TGF-β treatment (5 ng/mL) upregulates the expression of EMT-associated transcription factors such as Snail and Slug and downregulates the expression of epithelial markers such as ZO-1 and E-cadherin. Furthermore, treatment with TGF-β activates both Smad-dependent and Smad-independent signaling pathways, which subsides upon addition of Diphenyleneiodonium (DPI), a potent ROS inhibitor that inhibits NAPDH oxidase (NOX). TGF-β treatment enhanced cellular migration and invasion ability was diminished in the presence of ROS inhibitors. In addition, we also observed that ROS-mediated, TGF-β-induced EMT progression was inhibited using therapeutic candidates that target the key signal transduction mediators, including PI3K/AKT, ERK, and P38/MAPK. Accordingly, we demonstrated the involvement of redox biology (NOX2 and NOX4 mediate migration and invasion) in TGF-β-mediated EMT advancement and explored suitable therapeutic interventions.

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.

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