scholarly journals Role of ADAM17 in invasion and migration of CD133-expressing liver cancer stem cells after irradiation

Oncotarget ◽  
2016 ◽  
Vol 7 (17) ◽  
pp. 23482-23497 ◽  
Author(s):  
Sung Woo Hong ◽  
Wonhee Hur ◽  
Jung Eun Choi ◽  
Jung-Hee Kim ◽  
Daehee Hwang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Invasion And Migration ◽  
Liver Cancer Stem Cells ◽  
And Migration

Salinomycin suppresses tumorigenicity of liver cancer stem cells and Wnt/beta-catenin signaling

2020 ◽  
Vol 15 ◽  
Author(s):  
Qiuping Liu ◽  
Jinghui Sun ◽  
Qing Luo ◽  
Yang Ju ◽  
Guanbin Song
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Chemotherapy Resistance ◽  
Antitumor Agent ◽  
Beta Catenin ◽  
Liver Cancer Stem Cells

Background: Accumulating evidence has revealed the important role of cancer stem cells (CSCs) in driving tumor initiation and tumor relapse or metastasis. Therapeutic strategies that selectively target CSCs may be effective approaches to eliminate cancer. Salinomycin, an antitumor agent, was identified as a selective inhibitor of several types of CSCs. We previously reported that salinomycin inhibits the migration and invasiveness of liver cancer stem cells (LCSCs). Objective: This study was conducted to explore the role of salinomycin in supressing stemness properties of LCSCs and the mechanism. Methods: LCSCs were identified and enriched from MHCC97H cells. Salinomycin was used to treat LCSCs at the indicated concentrations. Sphere formation ability, chemotherapy resistance, expression of CSC surface markers, Young's modulus and tumorigenicity of LCSCs were assessed to evaluate the effect of salionmycin on LCSCs. The expression of β-catenin was evaluated by western blotting. LiCl was used to activate the Wnt/β-catenin signaling pathway. Results: Salinomycin suppresses the stemness properties of LCSCs. Moreover, salinomycin could also inhibit the activation of Wnt/β-catenin signaling in LCSCs. Nevertheless, the stemness properties of LCSCs could be recovered when Wnt/β-catenin signaling was activated by LiCl. Further studies demonstrated that salinomycin also significantly reduces the tumorigenicity of LCSCs in vivo by suppressing the Wnt/β-catenin signaling pathway. Conclusion: Salinomycin could suppress stemness properties and induce differentiation of LCSCs through the Wnt/β-catenin signaling pathway, which provides evidence that salinomycin may serve as a potential drug for liver cancer therapy targeting LCSCs in the clinic.

The Role of Liver Cancer Stem Cells in Donor Liver Allocation for Patients With Hepatocellular Carcinoma

2013 ◽  
Vol 125 (6) ◽  
pp. 24-30
Author(s):  
Jie Zhou ◽  
Zhenhua Hu ◽  
Zhiwei Li ◽  
Pengfei Yu ◽  
Jian Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Donor Liver ◽  
Liver Cancer Stem Cells ◽  
Liver Allocation

scholarly journals Role of microRNA miR-34a in liver cancer stem cells

2016 ◽  
Vol 11 (2) ◽  
pp. 333
Author(s):  
Lu-Lu Gong ◽  
Shu-Li Yang ◽  
Guo-Feng Zhang ◽  
Jia-Chengi Wu ◽  
Rui-Xin Lin
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Liver Tissue ◽  
Normal Liver ◽  
Cancer Tissue ◽  
Tissue Samples ◽  
Liver Cancer Stem Cells ◽  
Important Target

<p class="Abstract">The present study focuses on the role of microRNA miR-34a in liver cancer stem cells. Liver tissue samples were collected from the control and liver cancer patients. Immunohistochemistry experiment with CD90 antibodies suggests that the liver cancer stem cells were present in the liver cancer tissue samples. Interestingly, flow cytometry analysis followed by qRT-PCR confirmed that the CD90<sup>+</sup> cells also called as liver cancer stem cells shows expression of miR-34a at the levels of 30-80%, when compared with that of normal liver tissue samples. The present study concludes that the liver cancer stem cells shows high expression of miR-34a, which is the important target unique to liver cancer stem cells in order to design liver cancer stem cells-specific therapies.</p><p> </p>

scholarly journals HOTAIR Contributes to Stemness Acquisition of Cervical Cancer through Regulating miR-203 Interaction with ZEB1 on Epithelial-Mesenchymal Transition

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Wenying Zhang ◽  
Jing Liu ◽  
Qiongwei Wu ◽  
Yu Liu ◽  
Chengbin Ma
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cultured Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Cervical Cancer Cells ◽  
And Migration

Cervical cancer stem cells contribute respond to considerable recurrence and metastasis of patients with cervical cancer. The stemness properties were partly regulated by the interaction of lncRNAs and miRNAs. HOTAIR functions as an oncogenic lncRNA. Previous research studies revealed its role in regulating stemness properties in various cancers. However, the role of HOTAIR in cervical cancer stem cells is still unknown. Here, cisplatin-resistant and serum-free cultured cells exhibited stem cells properties. Cervical cancer stem cells exhibited greater invasion and migration compared with their parental cells, which was similar to cells overexpressing HOTAIR. HOTAIR was significantly overexpressed in cervical cancer stem cells, and knockdown of HOTAIR generated statistical downregulation of stemness markers. Additionally, HOTAIR expression was negatively correlated with the level of miR-203, which was found to be an inhibitory miRNA in regulating the expressions of stemness markers. Also, miR-203 expression was negatively correlated with ZEB1. These findings suggested that HOTAIR should be a positive contributor in stemness acquisition of cervical cancer cells, and this effect should correlate with the interaction with miR-203, which can be suppressed by ZEB1.

scholarly journals Liver Cancer Stem Cells

2008 ◽  
Vol 26 (17) ◽  
pp. 2800-2805 ◽  
Author(s):  
Stewart Sell ◽  
Hyam L. Leffert
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Liver Cancer Stem Cells ◽  
Liver Stem Cells ◽  
Carcinogenic Process ◽  
Liver Cancer Stem Cell ◽  
New Hypothesis

In an effort to review the evidence that liver cancer stem cells exist, two fundamental questions must be addressed. First, do hepatocellular carcinomas (HCC) arise from liver stem cells? Second, do HCCs contain cells that possess properties of cancer stem cells? For many years the finding of preneoplastic nodules in the liver during experimental induction of HCCs by chemicals was interpreted to support the hypothesis that HCC arose by dedifferentiation of mature liver cells. More recently, recognition of the role of small oval cells in the carcinogenic process led to a new hypothesis that HCC arises by maturation arrest of liver stem cells. Analysis of the cells in HCC supports the presence of cells with stem-cell properties (ie, immortality, transplantability, and resistance to therapy). However, definitive markers for these putative cancer stem cells have not yet been found and a liver cancer stem cell has not been isolated.

Sign in / Sign up

Export Citation Format

Share Document