Role of cancer stem cells in hepatocarcinogenesis

Wang, Bo; Jacob, Samson T.

doi:10.1186/gm225

Cited by 26 publications

(21 citation statements)

References 76 publications

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“…Furthermore, recruitment of progenitor cells has been shown to contribute to liver cancer formation in a preclinical model, and probably give rise to HCC as well as intrahepatic cholangiocarcinoma, supporting the view that progenitor cells in some cases have a critical role in the initiation and progression of liver cancers [48,88,89,93,94] . These findings might also support the hypothesis of genuine liver cancer stem cells that might be derived from HPCs [94][95][96] . The progenitor cells can also affect HCC progression through indirect contribution of growth factors.…”

Section: Hepatic Progenitor Cells and Liver Tumor Developmentsupporting

confidence: 82%

“…The progenitor cells can also affect HCC progression through indirect contribution of growth factors. In experimental rodent models with intrahepatic tumor implantation and concomitant liver resection, the presence of tumor seems to stimulate liver regeneration in major resected animals (> 70%) compared with resected animals without tumor, and this could possibly partly be attributed to the activation of progenitor like cells [25,95] . Similarly, in vitro and in vivo models testing the influence of progenitor cells on rodent HCC cells and experimental tumors indicate that the progenitor cells causes a "stemlike" expression profile in the HCC cells making them more resistant to chemotherapy and creating tumors that grow faster with greater invasive and metastatic potential.…”

Section: Hepatic Progenitor Cells and Liver Tumor Developmentmentioning

confidence: 99%

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Effect of liver regeneration on malignant hepatic tumors

Shi

Line

2014

WJG

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Liver regeneration after major surgery may activate occult micrometastases and facilitate tumor growth, leading to liver tumor recurrence. Molecular changes during liver regeneration can provide a microenvironment that stimulates intrahepatic tumor propagation through alterations in cellular signaling pathways, where activation and proliferation of mature hepatocytes, hepatic progenitor cells, non-parenchymal liver cells might favor both liver regeneration and tumor growth. This review highlights recent advances of tumor growth and development in the regenerating liver, possible mechanisms and clinical implications. Key words: Hepatocellular carcinoma; Colorectal cancer; Recurrence; Liver regeneration; Hepatic progenitor cell; Epithelial to mesenchymal transition Core tip: The liver has a unique capacity for regeneration after cellular damage or partial removal of tissue, and modern liver surgery relies on this property. Liver regeneration is a complex process involving a large array of growth factors, cytokines and cells to restore hepatic mass and function. Experimental and clinical data indicate that the regeneration signals facilitate the growth of both primary and secondary liver tumors and can alter their malignant potential. This is an important mechanism underlying recurrence after liver surgery. New therapeutic strategies founded on better insight into the relationship between liver regeneration and tumor biology are needed.Shi JH, Line PD. Effect of liver regeneration on malignant hepatic tumors.

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Section: Hepatic Progenitor Cells and Liver Tumor Developmentsupporting

confidence: 82%

Section: Hepatic Progenitor Cells and Liver Tumor Developmentmentioning

confidence: 99%

Effect of liver regeneration on malignant hepatic tumors

Shi

Line

2014

WJG

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“…Cancer stem cells, as TICs, play a key role in all stages of carcinogenesis (27). To confirm the contribution of TIF to cancer progression, we examined effect of TIF on the percentage of cancer stem cells in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Tumor Interstitial Fluid Promotes Malignant Phenotypes of Lung Cancer Independently of Angiogenesis

Li¹,

Li²,

Liu³

et al. 2015

Cancer Prevention Research

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Angiogenesis is necessary for cancer progression, but antiangiogenic therapy actually promotes tumor recurrence, progression, and metastasis. This study focused on the contribution of the tumor interstitial fluid (TIF) to lung cancer progression. TIF was isolated and quantified for 10 mg protein/mL. Malignant driver characteristics of TIF were examined by tumor-initiating cells (TIC), self-renewal, epithelial-mesenchymal transition (EMT), autophagy, and apoptosis in vitro. In vivo tumor model was used to investigate the mechanistic roles of TIF in lung cancer progression. In vitro, TIF exhibited distinct malignant driver characteristics, which led to increased numbers of TICs, increased selfrenewal and EMT, as well as to decreased autophagy and apoptosis under cell starvation conditions. In vivo, the contribution of TIF was similar, as judged by increased TICs indicated by the cancer stem cell marker Nanog, the proliferation marker proliferating cell nuclear antigen, and the EMT marker N-cadherin; TIF also increased the formation of pulmonary tumors. Interestingly, the blockers of inflammation, Na-K-ATPase, and aldosterone receptor decreased TIF-induced tumor progression but increased angiogenesis. Further, we found that the water content of the tissue was positively correlated with the levels of plasma 5-hydroxyindoleacetic acid or tissue aquaporin-1 but not with CD31. However, vadimezan reduced angiogenesis but promoted TIF-induced tumor progression. Our results suggested that TIF could provide better nutrition to the tumor than angiogenesis and that it could promote the development of malignant phenotypes of lung cancer independently of angiogenesis.

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“…Thus, other markers have been used, such as CD90, demonstrating that CD90 cells have high tumorigenic potential, unlike CD90 -cells. 40 …”

Section: Liver Cancermentioning

confidence: 99%