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pubmed, article, cancer, google, scholar, cas, wang, cells, stem, cell, central, fibroblasts, carcinoma, cancerassociated, hepatocellular, stemness, signaling, stat, hcc, liver, zhao, tumor, cafs, liu, chen, microenvironment, zhang, promote, pathway, promotes, cheng, properties, access, res, metastasis, nat, clin, yang, privacy, cookies, content, journal, paracrine, xiong, expression, selfrenewal, rev, zhu, luo, lin,

Topics {✒️}

hepatocyte growth factor c-met/fra1/hey1 signaling il-6/jak/stat3 signalling axis key tumor-promoting factor month download article/chapter ccl2 mediates cross-talk csc-related molecules serves il-6-stat3 axis mediates il-6/stat3/notch signaling pro-metastatic tumour microenvironment anti-cd24 antibody results hepatocellular carcinoma cells lee jm yuchong zhao & bin cheng cancer stem cells jak2/stat3 signaling pathway glioblastoma stem cells c-met pathway promotes stat3-mediated nanog regulation full article pdf human hepatocellular carcinoma liver cancer stem stem cell states cd24+ liver cells caf-derived hgf related subjects privacy choices/manage cookies stem cells stem cells 27 cd24+ cells isolated medema jp fgf-1/−3/fgfr4 signaling cd24+ hcc cells notch pathway promotes stat3 signaling pathway support tumor progress neck cancer progression interleukin-6 receptor antagonist sdf-1/cxcr4 axis molecular medicine aims maintain mesenchymal de sousa emf poor clinical outcomes c-met represents stem cell check access instant access stat3-mediated upregulation tgf-beta pathways de jong jh

Questions {❓}

• Gupta PB, Chaffer CL, Weinberg RA (2009) Cancer stem cells: mirage or reality?

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         headline:Cancer-associated fibroblasts promote the stemness of CD24+ liver cells via paracrine signaling
         description:Cancer stem cells (CSCs), which support tumor progress in hepatocellular carcinoma (HCC) developed in fibrotic or cirrhotic livers, are regulated by the tumor microenvironment. Cancer-associated fibroblasts (CAFs) are the major component of the tumor stroma in HCC; however, the mechanisms by which CAFs contribute to stemness maintenance remain largely unknown. Here, we found that the expression of CD24 was high in HCC tissues compared with adjacent normal liver tissues, and positively correlated with the poor prognosis and α-SMA expression in CAFs. CD24+ cells isolated from HCC cell lines exhibited stemness properties of self-renewal, chemotherapy resistance, metastasis, and tumorigenicity in NOD/SCID mice. Moreover, CAF-derived HGF and IL6 enhanced the stemness properties of CD24+ cells via activating STAT3 Tyr705 phosphorylation. Blockade of HGF/c-Met or IL6/IL6R signaling significantly abolished the effect of CAFs on stemness properties, which compromised the activation of STAT3 pathway in CD24+ cells. Meanwhile, knockdown of STAT3 in CD24+ cells notably attenuated CAF-induced stemness characteristics of CD24+ cells. Furthermore, in HCC patients, higher expression of phospho-STAT3 was also demonstrated to be positively correlated with poor clinical outcomes. In summary, HGF and IL6 secreted by CAFs promoted the stemness properties of CD24+ cells through the phosphorylation of STAT3 signaling, and targeting the paracrine pathways may provide a new therapeutic strategy for HCC.
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            Cancer-associated fibroblasts
            Hepatocellular carcinoma
            Interleukin-6
            Hepatocyte growth factor
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            Molecular Medicine
            Human Genetics
            Internal Medicine
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      headline:Cancer-associated fibroblasts promote the stemness of CD24+ liver cells via paracrine signaling
      description:Cancer stem cells (CSCs), which support tumor progress in hepatocellular carcinoma (HCC) developed in fibrotic or cirrhotic livers, are regulated by the tumor microenvironment. Cancer-associated fibroblasts (CAFs) are the major component of the tumor stroma in HCC; however, the mechanisms by which CAFs contribute to stemness maintenance remain largely unknown. Here, we found that the expression of CD24 was high in HCC tissues compared with adjacent normal liver tissues, and positively correlated with the poor prognosis and α-SMA expression in CAFs. CD24+ cells isolated from HCC cell lines exhibited stemness properties of self-renewal, chemotherapy resistance, metastasis, and tumorigenicity in NOD/SCID mice. Moreover, CAF-derived HGF and IL6 enhanced the stemness properties of CD24+ cells via activating STAT3 Tyr705 phosphorylation. Blockade of HGF/c-Met or IL6/IL6R signaling significantly abolished the effect of CAFs on stemness properties, which compromised the activation of STAT3 pathway in CD24+ cells. Meanwhile, knockdown of STAT3 in CD24+ cells notably attenuated CAF-induced stemness characteristics of CD24+ cells. Furthermore, in HCC patients, higher expression of phospho-STAT3 was also demonstrated to be positively correlated with poor clinical outcomes. In summary, HGF and IL6 secreted by CAFs promoted the stemness properties of CD24+ cells through the phosphorylation of STAT3 signaling, and targeting the paracrine pathways may provide a new therapeutic strategy for HCC.
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         Cancer-associated fibroblasts
         Hepatocellular carcinoma
         Interleukin-6
         Hepatocyte growth factor
         STAT3
         Molecular Medicine
         Human Genetics
         Internal Medicine
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