scholarly journals Casticin inhibits epithelial-mesenchymal transition of liver cancer stem cells of the SMMC-7721 cell line through downregulating Twist

2014 ◽  
Vol 7 (5) ◽  
pp. 1625-1631 ◽  
Author(s):  
MENG HE ◽  
XIAO-CHENG CAO ◽  
GUI-CHENG HE ◽  
XI-FENG SHENG ◽  
XIAO-HONG AI ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Cell Line ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Liver Cancer Stem Cells

Overexpression of miR-200a suppresses epithelial-mesenchymal transition of liver cancer stem cells

Tumor Biology ◽  
2014 ◽  
Vol 36 (4) ◽  
pp. 2447-2456 ◽  
Author(s):  
Jianlin Wang ◽  
Xisheng Yang ◽  
Bai Ruan ◽  
Bin Dai ◽  
Yuan Gao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Liver Cancer Stem Cells

scholarly journals Casticin inhibits self-renewal of liver cancer stem cells from the MHCC97 cell line

2014 ◽  
Vol 7 (6) ◽  
pp. 2023-2028 ◽  
Author(s):  
GUICHENG HE ◽  
XIAOCHENG CAO ◽  
MENG HE ◽  
XIFENG SHENG ◽  
YOUHUA WU ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Cell Line ◽  
Self Renewal ◽  
Liver Cancer Stem Cells

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 E-CADHERIN EXPRESSION DOWNREGULATION ELEVATES TUMOROGENIC POTENTIAL OF HUMAN COLON CANCER CELL LINE HCT116 VIA INCREASE IN CANCER STEM CELLS AMOUNT

2016 ◽  
Vol 15 (3) ◽  
pp. 6-14 ◽  
Author(s):  
M. D. Farmakovskaya ◽  
N. V. Khromova ◽  
B. P. Kopnin ◽  
P. B. Kopnin
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Line ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Cell Line ◽  
Human Colon ◽  
Colon Cancer Cell Line ◽  
Human Colon Cancer ◽  
Mesenchymal Transition ◽  
E Cadherin

Introduction. E-cadherin aberrant expression or complete loss is common for a number of human malignant neoplasms, and can be a launching mechanism of an epithelial-mesenchymal transition. Passing through epithelial-mesenchymal transition could in turn promote to the acquisition of so called cancer stem cell phenotype by the transformed cells. The objective of the present study is to reveal the influence of E-cadherin expression level on the amount of cancer stem cells in human colon cancer cell line HCT116. Materials and methods. We have created cell sublines with E-cadherin up- and downregulation and assessed the percentage of cancer stem cells using tumor formation assay, clonogenic assay; we also evaluated profile of cell pluripotency markers. Results and conclusion. We have shown that the proportion of cancer stem cells in human colon adenocarcinoma cell line HCT116 depends on the E-cadherin expression level. E-cadherin expression downregulation results in elevated expression of pluripotency genes and in the increase of proportion of cancer stem cells via activation of Wnt/ß-signalling pathway. E-cadherin upregulation has a reverse effect and decreases the amount of HCT116 cancer stem cells. Thus, E-cadherin expression restoration seems prospective in colorectal anticancer therapy.

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