Musashi2 Contributes to the Maintenance of CD44v6+ Liver Cancer Stem Cells via Notch1 Signaling Pathway

2019 ◽  
Author(s):  
Xiju Wang ◽  
Ronghua Wang ◽  
Shuya Bai ◽  
Si Xiong ◽  
Yawen Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Liver Cancer Stem Cells ◽  
Notch1 Signaling ◽  
Notch1 Signaling Pathway

scholarly journals ZBP-89 negatively regulates self-renewal of liver cancer stem cells via suppression of Notch1 signaling pathway

2020 ◽  
Vol 472 ◽  
pp. 70-80 ◽  
Author(s):  
Nuozhou Wang ◽  
Ming-yue Li ◽  
Yi Liu ◽  
Jianqing Yu ◽  
Jianwei Ren ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Self Renewal ◽  
Liver Cancer Stem Cells ◽  
Notch1 Signaling ◽  
Notch1 Signaling Pathway

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 Notch and Wnt/β-catenin signaling pathway play important roles in activating liver cancer stem cells

Oncotarget ◽  
2015 ◽  
Vol 7 (5) ◽  
pp. 5754-5768 ◽  
Author(s):  
Ronghua Wang ◽  
Qian Sun ◽  
Peng Wang ◽  
Man Liu ◽  
Si Xiong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Liver Cancer Stem Cells

scholarly journals Knockdown of miR-25 increases the sensitivity of liver cancer stem cells to TRAIL-induced apoptosis via PTEN/PI3K/Akt/Bad signaling pathway

2016 ◽  
Vol 49 (6) ◽  
pp. 2600-2610 ◽  
Author(s):  
Xiaoning Feng ◽  
Jingjin Jiang ◽  
Shaohua Shi ◽  
Haiyang Xie ◽  
Lin Zhou ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Liver Cancer Stem Cells ◽  
Induced Apoptosis

scholarly journals Musashi2 contributes to the maintenance of CD44v6+ liver cancer stem cells via notch1 signaling pathway

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Xiju Wang ◽  
Ronghua Wang ◽  
Shuya Bai ◽  
Si Xiong ◽  
Yawen Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Tissue Microarray ◽  
Migration And Invasion ◽  
Liver Cancer Stem Cells ◽  
Notch1 Signaling ◽  
And Function

Abstract Background Liver cancer stem cells (LCSCs) contribute to hepatocellular carcinoma (HCC) development, metastasis, and drug resistance. MSI2 and Notch1 signaling are involved in the maintenance of CSCs. However, it is unknown whether MSI2 and Notch1 are involved in the maintenance of CD44v6+ LCSCs. Therefore, we investigated the clinical significance and function of MSI2 and its relationship with Notch1 signaling in the maintenance of stemness properties in CD44v6+ LCSCs. Methods The expression of MSI2 and CD44v6 were detected by fresh specimens and a HCC tissue microarray. The tissue microarray containing 82 HCC samples was used to analyze the correlation between CD44v6 and MSI2. CD44v6+/− cells were isolated using microbeads sorting. We explored the roles of MSI2 and Notch1 signaling in CD44v6+ LCSCs by sphere formation assay, transwell assay, clone formation assay in vitro, and xenograft tumor models in vivo. A Notch RT2 PCR Array, Co-immunoprecipitation, and RNA-immunoprecipitation were used to further investigate the molecular mechanism of MSI2 in activating Notch1 signaling. Results Here, we found MSI2 expression was positively correlated with high CD44v6 expression in HCC tissues, and further correlated with tumor differentiation. CD44v6+ cells isolated from HCC cell lines exhibited increased self-renewal, proliferation, migration and invasion, resistance to Sorafenib and tumorigenic capacity. Both MSI2 and Notch1 signaling were elevated in sorted CD44v6+ cells than CD44v6- cells and played essential roles in the maintenance of stemness of CD44v6+ LCSCs. Mechanically, MSI2 directly bound to Lunatic fringe (LFNG) mRNA and protein, resulting in Notch1 activation. Conclusions Our results demonstrated that MSI2 maintained the stemness of CD44v6+ LCSCs by activating Notch1 signaling through the interaction with LFNG, which could be a potential molecular target for stem cell-targeted therapy for liver cancer.

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