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.

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.

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

scholarly journals Efficacy of Using Cancer Stem Cell Markers in Isolating and Characterizing Liver Cancer Stem Cells

2013 ◽  
Vol 22 (19) ◽  
pp. 2655-2664 ◽  
Author(s):  
George S. Wilson ◽  
Zenan Hu ◽  
Wei Duan ◽  
Aiping Tian ◽  
Xin M. Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Cancer Stem Cell ◽  
Stem Cell Markers ◽  
Cell Markers ◽  
Cancer Stem Cell Markers ◽  
Liver Cancer Stem Cells

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 A Novel Function for KLF4 in Modulating the De-Differentiation of EpCAM−/CD133− nonStem Cells into EpCAM+/CD133+ Liver Cancer Stem Cells in HCC Cell Line HuH7

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1198 ◽  
Author(s):  
Zeynep Firtina Karagonlar ◽  
Soheil Akbari ◽  
Mustafa Karabicici ◽  
Eren Sahin ◽  
Sanem Tercan Avci ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Cell Line ◽  
Tumor Cells ◽  
Cell Phenotype ◽  
High Plasticity ◽  
Liver Cancer Stem Cells

The complex and heterogeneous nature of hepatocellular carcinoma (HCC) hampers the identification of effective therapeutic strategies. Cancer stem cells (CSCs) represent a fraction of cells within tumors with the ability to self-renew and differentiate, and thus significantly contribute to the formation and maintenance of heterogeneous tumor mass. Increasing evidence indicates high plasticity in tumor cells, suggesting that non-CSCs could acquire stem cell properties through de-differentiation or reprogramming processes. In this paper, we reveal KLF4 as a transcription factor that can induce a CSC-like phenotype in non-CSCs through upregulating the EpCAM and E-CAD expression. Our studies indicated that KLF4 could directly bind to the promoter of EpCAM and increase the number of EpCAM+/CD133+ liver cancer stem cells (LCSCs) in the HuH7 HCC cell line. When KLF4 was overexpressed in EpCAM−/CD133− non-stem cells, the expressions of hepatic stem/progenitor cell genes such as CK19, EpCAM and LGR5 were significantly increased. KLF4 overexpressing non-stem cells exhibited greater cell viability upon sorafenib treatment, while the cell migration and invasion capabilities of these cells were suppressed. Importantly, we detected an increased membranous expression and colocalization of β-CAT, E-CAD and EpCAM in the KLF4-overexpressing EpCAM−/CD133− non-stem cells, suggesting that this complex might be required for the cancer stem cell phenotype. Moreover, our in vivo xenograft studies demonstrated that with a KLF4 overexpression, EpCAM−/CD133− non-stem cells attained an in vivo tumor forming ability comparable to EpCAM+/CD133+ LCSCs, and the tumor specimens from KLF4-overexpressing xenografts had increased levels of both the KLF4 and EpCAM proteins. Additionally, we identified a correlation between the KLF4 and EpCAM protein expressions in human HCC tissues independent of the tumor stage and differentiation status. Collectively, our data suggest a novel function for KLF4 in modulating the de-differentiation of tumor cells and the induction of EpCAM+/CD133+ LCSCs in HuH7 HCC cells.

scholarly journals PCGF2 and PCGF4 Opposite Drive Stem-like Properties in Hepatocellular Carcinoma

2021 ◽  
Author(s):  
Jinjing Hu ◽  
Yongqiang Zhou ◽  
Huan Feng ◽  
Yi Xie ◽  
Kuo Qi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
P38 Mapk ◽  
Cell Lines ◽  
Cell Counting ◽  
Stem Cell Population ◽  
Liver Cancer Stem Cells ◽  
Sphere Formation

Abstract Background: PCGF4 is highly expressed in liver cancer and can be used as a marker for liver cancer stem cells. However, PCGF2, a homologue of PCGF4, is not clear whether it is expressed in HCC, and whether it regulates the stemness of liver cancer stem cells.Methods: IHC and Western blot were used to detect the expression of PCGF2 and PCGF4 protein in human HCC tissues and cell lines. Flow cytometry and sphere formation were performed to detect the effect of PCGF2 or PCGF4 on the stem-like properties of liver cancer stem cells. Kaplan-Meier curves were conducted for OS and DFS. Cell viability was measured at the indicated time points using Cell Counting Kit-8. We performed KEGG analysis on these target genes through the cluster profiler package of the R language.Results: IHC results showed that PCGF2 was lower expressed in HCC, while PCGF4 was higher expressed in HCC compared with matched paracancerous, and this higher expression exhibited poor prognosis in HCC. Up regulation of PCGF2 was also accompanied with decreased stem-like properties and sphere formation in HCC cell lines. Interestingly, down regulating PCGF4 got the similar results as up regulating PCGF2. Furthermore, up regulating PCGF2 or down regulating PCGF4 cells performed more sensitivity to sorafenib. We also found that PCGF2 and PCGF4 oppositely regulated the drives stem-like properties by p38 MAPK signal pathway.Conclusion: PCGF2 was a novel negative regulator of LCSCs that inhibiting the stem cell population, reducing the sphere formation ability of liver cancer stem cells, and increasing the sensitivity of sorafenib by targeting p38 MAPK signaling. PCGF2 was supposed to be a novel therapeutic target for Liver cancer stem cell.

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