scholarly journals IL-6/STAT3 Signaling Contributes to Sorafenib Resistance in Hepatocellular Carcinoma Through Targeting Cancer Stem Cells [Corrigendum]

2020 ◽  
Vol Volume 13 ◽  
pp. 12253-12254
Author(s):  
Yu Li ◽  
Gang Chen ◽  
Zhijian Han ◽  
Huijuan Cheng ◽  
Liang Qiao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Stat3 Signaling

scholarly journals IL-6/STAT3 Signaling Contributes to Sorafenib Resistance in Hepatocellular Carcinoma Through Targeting Cancer Stem Cells

2020 ◽  
Vol Volume 13 ◽  
pp. 9721-9730
Author(s):  
Yu Li ◽  
Gang Chen ◽  
Zhijian Han ◽  
Huijuan Cheng ◽  
Liang Qiao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Stat3 Signaling

scholarly journals 4‐phenylbutyric acid promotes hepatocellular carcinoma via initiating cancer stem cells through activation of PPAR‐α

2021 ◽  
Vol 11 (4) ◽  
Author(s):  
Shu‐Zhen Chen ◽  
Yan Ling ◽  
Le‐Xing Yu ◽  
Yu‐Ting Song ◽  
Xiao‐Fei Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Phenylbutyric Acid

The multiple origin of cancer stem cells in hepatocellular carcinoma

2015 ◽  
Vol 39 ◽  
pp. S92-S97 ◽  
Author(s):  
Beatrice Anfuso ◽  
Korri E. El-Khobar ◽  
Caecilia H.C. Sukowati ◽  
Claudio Tiribelli
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Multiple Origin

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>

scholarly journals RACK1 Promotes Self-Renewal and Chemoresistance of Cancer Stem Cells in Human Hepatocellular Carcinoma through Stabilizing Nanog

Theranostics ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 811-828 ◽  
Author(s):  
Junxia Cao ◽  
Min Zhao ◽  
Jian Liu ◽  
Xueying Zhang ◽  
Yujun Pei ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Human Hepatocellular Carcinoma ◽  
Self Renewal

scholarly journals Increased Oxidative Phosphorylation Is Required for Stemness Maintenance in Liver Cancer Stem Cells from Hepatocellular Carcinoma Cell Line HCCLM3 Cells

2020 ◽  
Vol 21 (15) ◽  
pp. 5276 ◽  
Author(s):  
Ge Liu ◽  
Qing Luo ◽  
Hong Li ◽  
Qiuping Liu ◽  
Yang Ju ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Energy Metabolism ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Oxidative Phosphorylation ◽  
Carcinoma Cell ◽  
Hepatocellular Carcinoma Cell Line ◽  
Hepatocellular Carcinoma Cell ◽  
The Relationship

Cancer stem cells (CSCs) are considered to be the main cause of tumor recurrence, metastasis, and an unfavorable prognosis. Energy metabolism is closely associated with cell stemness. However, how the stemness of liver cancer stem cells (LCSCs) is regulated by metabolic/oxidative stress remains poorly understood. In this study, we compare the metabolic differences between LCSCs and the hepatocellular carcinoma cell line HCCLM3, and explore the relationship between metabolism and LCSC stemness. We found that LCSCs from the hepatocellular carcinoma cell HCCLM3 exhibited more robust glucose metabolism than HCCLM3, including glycolysis, oxidative phosphorylation (OXPHOS), and pyruvate produced by glycolysis entering mitochondria for OXPHOS. Moreover, 2-deoxy-D-glucose (2-DG) enhanced the LCSC stemness by upregulating OXPHOS. In contrast, Mdivi-1 reduced the levels of OXPHOS and weakened the stemness by inhibiting mitochondrial fission. Together, our findings clarify the relationship between energy metabolism and LCSC stemness and may provide theoretical guidance and potential therapeutic approaches for liver cancer.

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