scholarly journals Absence of EpCAM in Cervical Cancer Cells Is Involved in Slug-induced Epithelial-mesenchymal Transition

2020 ◽  
Author(s):  
Xian Liu ◽  
Feng Qian ◽  
Yanru Zhang ◽  
Pengsheng Zheng ◽  
Nan Cui
Keyword(s):  
Cervical Cancer ◽  
Cell Motility ◽  
Cancer Cells ◽  
Negative Correlation ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Suppression Effect ◽  
Epcam Expression ◽  
Cervical Cancer Cells ◽  
E Cadherin

Abstract Background: Slug (Snai2) is a pivotal player in initiating epithelial-mesenchymal transition (EMT) through its trans-suppression effect on E-cadherin in various normal and malignant cells. In this study. The positive effect of Slug on promoting cell motility and metastasis in cervical cancer was further confirmed in this study.Methods: RNA-Seq was performed to explore the potential molecules that participate in Slug-mediated EMT in cervical cancer cells. The negative correlation between Slug and EpCAM expression in cervical cancer cells was detected in this study, and linked them with in vitro migration and invasion assay, in vivo metastasis experiments, luciferase reporter assay and Chromatin immunoprecipitation.Results: Transcriptome sequencing analysis revealed that epithelial cell adhesion molecule (EpCAM) was significantly decreased in Slug-overexpressing SiHa cells. Simultaneously, an absence of EpCAM expression was observed in Slug-overexpressing cells. Further studies revealed the trans-suppression effect of Slug on EpCAM through its binding to the E-boxes in the proximal promoter region of EpCAM in cervical cancer cells. Restoring EpCAM in Slug-overexpressing cells by transiently transfecting an EpCAM recombinant plasmid attenuated cell motility and promoted cell growth. Moreover, the negative correlation between Slug and EpCAM expression in human squamous cervical carcinoma (SCC) samples was verified by using Pearson correlation analysis.Conclusions: These results demonstrated that the absence of EpCAM under Slug expression in cervical cancer cells probably participated in Slug-regulated EMT and further promoted tumor metastasis. Additionally, this study supports a potential way for Slug to initiate EMT progression in cervical cancer cells in addition to inhibiting E-cadherin.

scholarly journals Absence of EpCAM in cervical cancer cells is involved in slug induced epithelial-mesenchymal transition

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xian Liu ◽  
Qian Feng ◽  
Yanru Zhang ◽  
PengSheng Zheng ◽  
Nan Cui
Keyword(s):  
Cervical Cancer ◽  
Cell Motility ◽  
Cancer Cells ◽  
Negative Correlation ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Suppression Effect ◽  
Epcam Expression ◽  
Cervical Cancer Cells ◽  
E Cadherin

Abstract Background Slug (Snai2) is a pivotal player in initiating epithelial-mesenchymal transition (EMT) through its trans-suppression effect on E-cadherin in various normal and malignant cells. In this study, the positive effect of Slug on promoting cell motility and metastasis in cervical cancer was further confirmed in this study. Methods RNA-Seq was performed to explore the potential molecules that participate in Slug-mediated EMT in cervical cancer cells. The negative correlation between Slug and EpCAM expression in cervical cancer cells was detected in this study, and linked them with in vitro migration and invasion assay, in vivo metastasis experiments, luciferase reporter assay and Chromatin immunoprecipitation. Results Transcriptome sequencing analysis revealed that epithelial cell adhesion molecule (EpCAM) was significantly decreased in Slug-overexpressing SiHa cells. Simultaneously, an absence of EpCAM expression was observed in Slug-overexpressing cells. Further studies revealed the trans-suppression effect of Slug on EpCAM through its binding to the E-boxes in the proximal promoter region of EpCAM in cervical cancer cells. Restoring EpCAM in Slug-overexpressing cells by transiently transfecting an EpCAM recombinant plasmid attenuated cell motility and promoted cell growth. Moreover, the negative correlation between Slug and EpCAM expression in human squamous cervical carcinoma (SCC) samples was verified by using Pearson correlation analysis. Conclusions These results demonstrated that the absence of EpCAM under Slug expression in cervical cancer cells probably participated in Slug-regulated EMT and further promoted tumor metastasis. Additionally, this study supports a potential way for Slug to initiate EMT progression in cervical cancer cells in addition to inhibiting E-cadherin.

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.

1 E-Cadherin knockdown induces cancer stem cell-like phenotype and drug resistance

2021 ◽  
Author(s):  
Anuka Sharma ◽  
Harmandeep Kaur ◽  
Renaissa De ◽  
Radhika Srinivasan ◽  
Arnab Pal ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Drug Resistance ◽  
Stem Cell ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Stem Cell Marker ◽  
Mesenchymal Transition ◽  
Cytotoxicity Studies ◽  
Cervical Cancer Cells ◽  
E Cadherin

Cervical cancer is one of the leading causes of mortality amongst women in developing countries and therapy resistance is the main reason for its treatment failure. Recent advances suggest that cancer stem cells (CSCs) are critically involved in regulating the chemo resistant behavior of cervical cancer cells. In our study the CSC phenotype cells were isolated and the expression of stem cell marker and epithelial-mesenchymal transition (EMT) associated gene was confirmed by various assays. However, these CSC phenotype cells cannot be cultured for further cytotoxicity studies. So, we tried to establish a CSC model in cervical cancer cells. We performed the siRNA-mediated knockdown of E-cadherin (E-cad) in these cells and studied EMT associated stem cell-like properties in them. We also performed dose dependent cell viability assay using clinically relevant drugs such as cisplatin, cyclopamine and GANT58 to analyze the drug resistant behavior of these cancer cells. We found that E-cad knockdown induces EMT in cervical cancer cells imparting stem-cell like characteristics along with enhanced tumorsphere formation, migration, invasion ability and drug resistance. This is the first study to establish a CSC model in cervical cancer cells by knockdown of E-cad which can be utilized for development of anti-cancer therapies.

scholarly journals Retraction Note to: miR-484 suppresses proliferation and epithelial–mesenchymal transition by targeting ZEB1 and SMAD2 in cervical cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yang Hu ◽  
Hong Xie ◽  
Yankun Liu ◽  
Weiying Liu ◽  
Min Liu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Cervical Cancer Cells ◽  
Retraction Notice

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12935-021-01958-0

Human papillomavirus oncoproteins differentially modulate epithelial-mesenchymal transition in 5-FU-resistant cervical cancer cells

Tumor Biology ◽  
2016 ◽  
Vol 37 (10) ◽  
pp. 13137-13154 ◽  
Author(s):  
Kanchan Vishnoi ◽  
Sutapa Mahata ◽  
Abhishek Tyagi ◽  
Arvind Pandey ◽  
Gaurav Verma ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Cervical Cancer Cells

scholarly journals APMAP Promotes Epithelial-Mesenchymal Transition and Metastasis of Cervical Cancer Cells by Activating the Wnt/β-catenin Pathway

2021 ◽  
Vol 12 (20) ◽  
pp. 6265-6273
Author(s):  
Xiuting Zhu ◽  
Zijin Xiang ◽  
Lingxiao Zou ◽  
Xueru Chen ◽  
Xiangdong Peng ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Epithelial 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.

scholarly journals Crinamine Induces Apoptosis and Inhibits Proliferation, Migration, and Angiogenesis in Cervical Cancer SiHa Cells

Biomolecules ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 494 ◽  
Author(s):  
Khumkhrong ◽  
Piboonprai ◽  
Chaichompoo ◽  
Pimtong ◽  
Khongkow ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Mechanism Of Action ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Chemoprevention ◽  
Bioactive Compound ◽  
Perennial Herb ◽  
Mesenchymal Transition ◽  
Cervical Cancer Cells

Crinum asiaticum is a perennial herb widely distributed in many warmer regions, including Thailand, and is well-known for its medicinal and ornamental values. Crinum alkaloids contain numerous compounds, such as crinamine. Even though its mechanism of action is still unknown, crinamine was previously shown to possess anticancer activity. In this study, we demonstrate that crinamine was more cytotoxic to cervical cancer cells than normal cells. It also inhibited anchorage-independent tumor spheroid growth more effectively than existing chemotherapeutic drugs carboplatin and 5-fluorouracil or the CDK9 inhibitor FIT-039. Additionally, unlike cisplatin, crinamine induced apoptosis without promoting DNA double-strand breaks. It suppressed cervical cancer cell migration by inhibiting the expression of positive regulators of epithelial-mesenchymal transition SNAI1 and VIM. Importantly, crinamine also exerted anti-angiogenic activities by inhibiting secretion of VEGF-A protein in cervical cancer cells and blood vessel development in zebrafish embryos. Gene expression analysis revealed that its mechanism of action might be attributed, in part, to downregulation of cancer-related genes, such as AKT1, BCL2L1, CCND1, CDK4, PLK1, and RHOA. Our findings provide a first insight into crinamine's anticancer activity, highlighting its potential use as an alternative bioactive compound for cervical cancer chemoprevention and therapy.

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