scholarly journals MicroRNA-31 suppresses the self-renewal capability of α2δ1+ liver tumor-initiating cells by targeting ISL1

Oncotarget ◽  
2017 ◽  
Vol 8 (50) ◽  
pp. 87647-87657 ◽  
Author(s):  
Yuan Zhang ◽  
Wei Zhao ◽  
Haibo Han ◽  
Sheng Li ◽  
Dongji Chen ◽  
...  
Keyword(s):  
Liver Tumor ◽  
The Self ◽  
Tumor Initiating Cells ◽  
Self Renewal

scholarly journals The long noncoding RNA lncZic2 drives the self-renewal of liver tumor–initiating cells via the protein kinase C substrates MARCKS and MARCKSL1

2018 ◽  
Vol 293 (21) ◽  
pp. 7982-7992 ◽  
Author(s):  
Zhenzhen Chen ◽  
Yating Liu ◽  
Lintong Yao ◽  
Shiying Guo ◽  
Yanfeng Gao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Liver Cancer ◽  
Liver Tumor ◽  
Noncoding Rna ◽  
The Self ◽  
Tumor Initiating Cells ◽  
Self Renewal ◽  
Kinase C

Liver tumor–initiating cells (TICs) form small subsets of cells in hepatocellular tumors and account for tumorigenesis, metastasis, recurrence, and drug resistance. Recently, we found that the transcription factor Zic family member 2 (ZIC2) is highly expressed in liver TICs and required for their self-renewal. However, the molecular mechanisms underlying self-renewal of liver TICs remain unclear. Here, using expression profiling and CRISPR-interference assays with clinical samples of human liver cancers, we identified a long noncoding RNA (lncRNA), lncZic2, that is located near the ZIC2 locus and was highly expressed in liver cancer and liver TICs. We found that lncZic2 is required for the self-renewal of liver TICs in a ZIC2-independent manner. lncZic2 drove the expression of myristoylated alanine-rich protein kinase C substrate (MARCKS) and MARCKS-like 1 (MARCKSL1), whose expression levels were increased during liver tumorigenesis and liver TIC self-renewal. Mechanistically, lncZic2 interacted with BRM/SWI2-related gene 1 (BRG1) and recruited this transcriptional regulator to the promoters of the MARCKS and MARCKSL1 gene, which activated expression of these genes. Moreover, we noted that depletion of lncZic2 and BRG1 decreases MARCKS and MARCKSL1 expression and diminishes liver TIC levels. In conclusion, lncZic2 is required for the self-renewal of liver TICs by up-regulating MARCKS and MARCKSL1 gene expression via the transcription factor BRG1. Our findings suggest that the lncZic2–BRG1–MARCKS/MARCKSL1 signaling cascade might be a potential target for eliminating liver TICs in the management of liver cancer.

miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

2020 ◽  
Author(s):  
Shuping Qu ◽  
Xiaobing Zhang ◽  
Hengwei Fan ◽  
Yue Wu ◽  
Jian Zhai ◽  
...  
Keyword(s):  
Liver Tumor ◽  
Cohort Analysis ◽  
The Self ◽  
Tumor Initiating Cells ◽  
Self Renewal ◽  
Sorafenib Treatment ◽  
The Impact

Abstract Background: Increasing evidence shows that liver tumor-initiating cells (T-ICs) closely associated with the progression, metastasis, recurrence and chemo-resistance of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver T-ICs remains unclear. The purpose of our study was to explore the role of miR-361-3p in the expansion of liver T-ICs and the potential molecular mechanism.Results: Flow cytometry analysis was performed to isolate CD24+, CD133+ or EpCAM+ cells from primary HCC cells or HCC cell lines. Real-time PCR was used to detect the expression of miR-361-3p in liver T-ICs. The impact of miR-361-3p on liver T-ICS expansion was investigated both in vivo and in vitro. The correlation between miR-361-3p expression and TACE (transcatheter arterial chemoembolization) or sorafenib benefits in HCC was evaluated in patient cohorts. miR-361-3p expression is upregulated in liver T-ICs. Knockdown of miR-361-3p impairs the self-renewal and tumorigenicity liver T-ICs. Conversely, forced miR-361-3p expression enhances the self-renewal and tumorigenicity liver T-ICs. Mechanistically, miR-361-3p directly targets SOX1 via binding its 3’-UTR in liver T-ICs. Moreover, miR-361-3p knockdown hepatoma cells are more sensitive to cisplatin or sorafenib treatment. Clinical cohort analysis demonstrates that miR-361-3p low HCC patients are benefited from TACE or sorafenib treatment. Conclusions: Our findings revealed the crucial role of the miR-361-3p in liver T-IC expansion and TACE or sorafenib response, rendering miR-361-3p an optimal target for the prevention and intervention in HCC.

scholarly journals SAMMSON drives the self-renewal of liver tumor initiating cells through EZH2-dependent Wnt/β-catenin activation

Oncotarget ◽  
2017 ◽  
Vol 8 (61) ◽  
pp. 103785-103796 ◽  
Author(s):  
Xiaopeng Li ◽  
Ming Li ◽  
JiaLi Chen ◽  
Hua Dai ◽  
Liang Wang ◽  
...  
Keyword(s):  
Liver Tumor ◽  
The Self ◽  
Tumor Initiating Cells ◽  
Self Renewal

scholarly journals 245 DYRK1a Modulates the Self-renewal Capacity of Neural Stem Cells and Tumor Initiating Cells: Targetting the Achilles Heels of EGFR Addicted Glioblastomas

2012 ◽  
Vol 48 ◽  
pp. S60
Author(s):  
P. Sanchez Gomez ◽  
N. Pozo ◽  
C. Zahonero ◽  
P. Fernandez ◽  
A. Perez ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
The Self ◽  
Tumor Initiating Cells ◽  
Self Renewal

scholarly journals miR-96 Regulates Liver Tumor-Initiating Cells Expansion and Sorafenib Resistance

2020 ◽  
Author(s):  
Yonggang Huang ◽  
Jin Zhang ◽  
Wei Dong ◽  
Huiping Peng ◽  
Maolin Gu ◽  
...  
Keyword(s):  
Liver Tumor ◽  
Underlying Mechanism ◽  
Tumor Initiating Cells ◽  
Self Renewal ◽  
Sorafenib Treatment ◽  
Functional Studies ◽  
Optimal Target ◽  
The Impact

Abstract Background Liver tumor-initiating cells (T-ICs) contribute to tumorigenesis, progression, recurrence and drug resistance of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver T-ICs remains unclear. Methods Real-time PCR was used to detect the expression of miR-96 in liver tumor-initiating cells (T-ICs). The impact of miR-96 on liver T-ICs expansion was investigated both in vivo and in vitro . The correlation between miR-96 expression and sorafenib benefits in HCC was further evaluated in patient-derived xenografts (PDXs). Results Our finding shows that miR-96 is upregulated in liver T-ICs. Functional studies revealed that forced miR-96 promotes liver T-ICs self-renewal and tumorigenesis. Conversely, knockdown miR-96 inhibits liver T-ICs self-renewal and tumorigenesis. Mechanistically, miR-96 downregulates SOX6 via its mRNA 3’UTR in liver T-ICs. Furthermore, the miR-96 expression determines the responses of hepatoma cells to sorafenib treatment. Analysis of patient-derived xenografts (PDXs) further demonstrated that the miR-96 may predict sorafenib benefits in HCC patients. Conclusion Our findings revealed the crucial role of the miR-96 in liver T-ICs expansion and sorafenib response, rendering miR-96 as an optimal target for the prevention and intervention of HCC.

scholarly journals Circular RNA circGTIC1 drives gastric TIC self-renewal to initiate gastric tumorigenesis and metastasis

2019 ◽  
Author(s):  
Liyan Wang ◽  
Bin Li ◽  
Xuhua Xiao ◽  
Xiaoyuan Yi ◽  
Feifei He
Keyword(s):  
Gastric Cancer ◽  
Chromatin Remodeling ◽  
Circular Rna ◽  
The Self ◽  
Gastric Tumor ◽  
Dependent Manner ◽  
Tumor Initiating Cells ◽  
Self Renewal ◽  
Chromatin Remodeling Complex ◽  
The World

AbstractGastric cancer is one of the most serious cancers all over the world. Gastric tumor initiating cells (TIC) account for gastric tumorigenesis and metastasis. Here we identified circGTIC1 as a highly expressed circRNA in gastric cancer and gastric TICs. circGTIC1 knockout inhibited the self-renewal of gastric TICs and metastasis, and its overexpression activated gastric TICs. circGTIC1 drove the expression of Sox8 and exerted its role via Sox8-dependent manner. circGTIC1 associated with Ino80 chromatin remodeling complex, and recruited Ino80 complex to Sox8 promoter, finally initiated Sox8 expression. Our work revealed a novel circRNA to regulate gastric tumorigenesis and gastric TICs, adding a new layer for gastric TIC regulation and circRNA functions. CircGTIC1 plays a central role in gastric TIC self-renewal and metastasis. circGTIC1 drives the expression of Sox8 through recruiting Ino80 complex to Sox8 promoter. circGTIC1-Ino80-Sox8 axis can be used for gastric tumor and gastric TIC targeting. Our work revealed a novel circRNA to regulate gastric tumorigenesis and gastric TICs, adding a new layer for gastric TIC regulation and circRNA functions

Abstract 2445: CD24+liver tumor-initiating cells drives self-renewal and tumor initiation through Stat3-mediated Nanog regulation

2011 ◽  
Author(s):  
Kin Wah Lee ◽  
Antonia Castilho ◽  
Vincent Chi-Ho Cheung ◽  
Kwan Ho Tang ◽  
Stephanie Ma ◽  
...  
Keyword(s):  
Liver Tumor ◽  
Tumor Initiation ◽  
Tumor Initiating Cells ◽  
Self Renewal

scholarly journals circular RNA cia-MAF drives self-renewal and metastasis of liver tumor-initiating cells via transcription factor MAFF

2021 ◽  
Author(s):  
Zhenzhen Chen ◽  
Tiankun Lu ◽  
Lan Huang ◽  
Zhiwei Wang ◽  
Zhongyi Yan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Liver Tumor ◽  
Circular Rna ◽  
Tumor Initiating Cells ◽  
Self Renewal
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