Combination PARP and HDAC inhibition as a therapeutic strategy targeting liver cancer stem cells?

2016 ◽  
Vol 5 (5) ◽  
pp. 60-60 ◽  
Author(s):  
Catherine E. Willoughby ◽  
Helen L. Reeves
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Therapeutic Strategy ◽  
Hdac Inhibition ◽  
Liver Cancer Stem Cells

scholarly journals The inhibition of ABCB1/MDR1 or ABCG2/BCRP enables doxorubicin to eliminate liver cancer stem cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wang Yin ◽  
Dongxi Xiang ◽  
Tao Wang ◽  
Yumei Zhang ◽  
Cuong V. Pham ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
High Performance ◽  
Annexin V ◽  
Intracellular Concentration ◽  
Liver Cancer Stem Cells ◽  
Chemotherapy Agent ◽  
Future Strategy ◽  
Annexin V Assay

AbstractTwo ATP-binding cassette transporters, ABCB1/MDR1 and ABCG2/BCRP, are considered the most critical determinants for chemoresistance in hepatocellular carcinoma. However, their roles in the chemoresistance in liver cancer stem cells remain elusive. Here we explored the role of inhibition of MDR1 or ABCG2 in sensitizing liver cancer stem cells to doxorubicin, the most frequently used chemotherapeutic agent in treating liver cancer. We show that the inhibition of MDR1 or ABCG2 in Huh7 and PLC/PRF/5 cells using either pharmacological inhibitors or RNAi resulted in the elevated level of intracellular concentration of doxorubicin and the accompanied increased apoptosis as determined by confocal microscopy, high-performance liquid chromatography, flow cytometry, and annexin V assay. Notably, the inhibition of MDR1 or ABCG2 led to the reversal of the chemoresistance, as evident from the enhanced death of the chemoresistant liver cancer stem cells in tumorsphere-forming assays. Thus, the elevation of effective intracellular concentration of doxorubicin via the inhibition of MDR1 or ABCG2 represents a promising future strategy that transforms doxorubicin from a traditional chemotherapy agent into a robust killer of liver cancer stem cells for patients undergoing transarterial chemoembolization.

MK2206 overcomes the resistance of human liver cancer stem cells to sorafenib by inhibition of pAkt and upregulation of pERK

Tumor Biology ◽  
2015 ◽  
Vol 37 (6) ◽  
pp. 8047-8055 ◽  
Author(s):  
Beibei Zhai ◽  
Xiaofeng Zhang ◽  
Bin Sun ◽  
Lu Cao ◽  
Linlin Zhao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Human Liver ◽  
Liver Cancer Stem Cells ◽  
Human Liver Cancer

The clinical, prognostic and therapeutic significance of liver cancer stem cells and their markers

2021 ◽  
pp. 101664
Author(s):  
Izabela Zarębska ◽  
Arkadiusz Gzil ◽  
Justyna Durślewicz ◽  
Damian Jaworski ◽  
Paulina Antosik ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Liver Cancer Stem Cells

scholarly journals Inhibition of β‑catenin protein expression by triptolide affects self-renewal of liver cancer stem cells

2015 ◽  
Vol 10 (2) ◽  
pp. 455 ◽  
Author(s):  
Jian-Bo Zhou ◽  
Gang Peng ◽  
Yu-Cheng Jia ◽  
Jun Li ◽  
Jia Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Inhibitory Concentration ◽  
The Self ◽  
Tripterygium Wilfordii ◽  
Self Renewal ◽  
Liver Cancer Stem Cells ◽  
Novel Agent

<p>The present study demonstrates the effects of triptolide, one of the constituents from Tripterygium wilfordii, on the self‑renewal capacity of human hepatocellular carcinoma. The investigation revealed that triptolide markedly prevented the proliferation of liver cancer stem cells (LCSCs). For the LCSCs the minimum inhibitory concentration of triptolide was 0.6 μM. There was a significant and obvious decrease in the capacity of LCSCs to form self-sphere. Furthermore, triptolide reduced the sphere-forming capacity of LCSCs along with inhibition of β‑catenin expression. However, the exposure of triptolide-treated cells to lithium chloride, an activator the Wnt/β-catenin signaling pathway, reversed the triptolide-induced inhibition of β-catenin expression and inhibited the self-renewal capacity. Therefore, triptolide effectively eradicates LCSCs through the inhibition of β-catenin protein and may act as a novel agent for the treatment of hepatocellular carcinoma.</p><p> </p>

lncARSR promotes liver cancer stem cells expansion via STAT3 pathway

Gene ◽  
2019 ◽  
Vol 687 ◽  
pp. 73-81 ◽  
Author(s):  
Cheng Yang ◽  
Wen-chang Cai ◽  
Zhi-tao Dong ◽  
Jun-wu Guo ◽  
Yi-jun Zhao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Stat3 Pathway ◽  
Liver Cancer Stem Cells

scholarly journals Liver cancer stem cells are selectively enriched by low-dose cisplatin

2014 ◽  
Vol 47 (6) ◽  
pp. 478-482 ◽  
Author(s):  
H. Zhang ◽  
W.J. Chang ◽  
X.Y. Li ◽  
N. Zhang ◽  
J.J. Kong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Low Dose ◽  
Liver Cancer Stem Cells

The Wnt/β-catenin pathway is activated by miR-1246 in liver cancer stem cells

2016 ◽  
Vol 5 (S7) ◽  
pp. S1457-S1460 ◽  
Author(s):  
Melanie A. Eshelman ◽  
Gregory S. Yochum
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Liver Cancer Stem Cells
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