Cancer-associated fibroblasts promote the stemness of CD24+ liver cells via paracrine signaling

Li, Yawen; Wang, Ronghua; Xiong, Si; Wang, Xiju; Zhao, Zhenxiong; Bai, Shuya; Wang, Yun; Zhao, Yuchong; Cheng, Bin

doi:10.1007/s00109-018-1731-9

Cited by 60 publications

(53 citation statements)

References 44 publications

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“…Thus, RvD1 may be a potential agent to inhibit many cancers dependent on cancer stem cells such as hepatocellular carcinoma ( Sun et al, 2019 ). CAFs-derived COMP induced EMT and cancer stem cell-like properties to promote invasion and metastasis of HCC ( Sun et al, 2019 ), which was in accordance with previous findings that IL-6 secreted by CAFs confers stem-like properties in HCC via the upregulation of stemness-correlated transcription factors including Sox2, Oct4 and Nanog ( Li, Wang, Xiong, et al, 2019 ).…”

Section: Therapeutic Approachessupporting

confidence: 91%

Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

113

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Inflammation in the tumor microenvironment is a hallmark of cancer and is recognized as a key characteristic of carcinogens. However, the failure of resolution of inflammation in cancer is only recently being understood. Products of arachidonic acid and related fatty acid metabolism called eicosanoids, including prostaglandins, leukotrienes, lipoxins, and epoxyeicosanoids, critically regulate inflammation, as well as its resolution. The resolution of inflammation is now appreciated to be an active biochemical process regulated by endogenous specialized pro-resolving lipid autacoid mediators which combat infections and stimulate tissue repair/regeneration. Environmental and chemical human carcinogens, including aflatoxins, asbestos, nitrosamines, alcohol, and tobacco, induce tumor-promoting inflammation and can disrupt the resolution of inflammation contributing to a devastating global cancer burden. While mechanisms of carcinogenesis have focused on genotoxic activity to induce mutations, nongenotoxic mechanisms such as inflammation and oxidative stress promote genotoxicity, proliferation, and mutations. Moreover, carcinogens initiate oxidative stress to synergize with inflammation and DNA damage to fuel a vicious feedback loop of cell death, tissue damage, and carcinogenesis. In contrast, stimulation of resolution of inflammation may prevent carcinogenesis by clearance of cellular debris via macrophage phagocytosis and inhibition of an eicosanoid/cytokine storm of pro-inflammatory mediators. Controlling the host inflammatory response and its resolution in carcinogen-induced cancers will be critical to reducing carcinogen-induced morbidity and mortality. Here we review the recent evidence that stimulation of resolution of inflammation, including pro-resolution lipid mediators and soluble epoxide hydrolase inhibitors, may be a new chemopreventive approach to prevent carcinogen-induced cancer that should be evaluated in humans.

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Section: Therapeutic Approachessupporting

confidence: 91%

Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

113

View full text Add to dashboard Cite

show abstract

“…In addition, CAF can recruit regulatory DCs through IL-6-mediated STAT3 activation and educate them to obtain a tolerogenic phenotype and up-regulate Treg production by secreting TGF-β in the tumor microenvironment [83]. In summary, CAFs play an important role in the development and progression of cancer cells and targeting CAFs may be effective in treating fibrosis and preventing HCC progression (Tables 1, [84][85][86][87][88][89][90].…”

Section: Cancer-associated Fibroblastsmentioning

confidence: 99%

Current perspectives on the immunosuppressive tumor microenvironment in hepatocellular carcinoma: challenges and opportunities

et al. 2019

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Incidence of hepatocellular carcinoma (HCC) is on the rise due to the prevalence of chronic hepatitis and cirrhosis. Although there are surgical and chemotherapy treatment avenues the mortality rate of HCC remains high. Immunotherapy is currently the new frontier of cancer treatment and the immunobiology of HCC is emerging as an area for further exploration. The tumor microenvironment coexists and interacts with various immune cells to sustain the growth of HCC. Thus, immunosuppressive cells play an important role in the anti-tumor immune response. This review will discuss the current concepts of immunosuppressive cells, including tumor-associated macrophages, marrow-derived suppressor cells, tumor-associated neutrophils, cancer-associated fibroblasts, and regulatory T cell interactions to actively promote tumorigenesis. It further elaborates on current treatment modalities and future areas of exploration.

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“…Lau et al . elucidated that CAFs-derived HGF expanded liver tumor-initiating cells by regulating c-Met/FRA1/HEY1/ERK cascade [ 55 , 56 ]. Focusing on CD24 + HCC cells, Li et al .…”

Section: Cafs In Hccmentioning

confidence: 99%

“…Focusing on CD24 + HCC cells, Li et al . emphasized that CAFs induced the stemness via HGF- and IL-6-activated STAT3 pathway in vitro and in vivo [ 56 ]. Consistently, Xiong et al .…”

Section: Cafs In Hccmentioning

confidence: 99%

Identifying cancer-associated fibroblasts as emerging targets for hepatocellular carcinoma

Zhang

Song

et al. 2020

Cell Biosci

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The tumor microenvironment (TME) is a complex multicellular functional compartment that includes fibroblasts, myofibroblasts, endothelial cells, immune cells, and extracellular matrix (ECM) elements. The microenvironment provides an optimum condition for the initiation, growth, and dissemination of hepatocellular carcinoma (HCC). As one of the critical and abundant components in tumor microenvironment, cancer-associated fibroblasts (CAFs) have been implicated in the progression of HCC. Through secreting various growth factors and cytokines, CAFs contribute to the ECM remodeling, stem features, angiogenesis, immunosuppression, and vasculogenic mimicry (VM), which reinforce the initiation and development of HCC. In order to restrain the CAFs-initiated HCC progression, current strategies include targeting specific markers, engineering CAFs with tumor-suppressive phenotype, depleting CAFs’ precursors, and repressing the secretions or downstream signaling. In this review, we update the emerging understanding of CAFs in HCC, with particular emphasis on cellular origin, phenotypes, biological functions and targeted strategies. It provides insights into the targeting CAFs for HCC treatment.

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Cancer-associated fibroblasts promote the stemness of CD24+ liver cells via paracrine signaling

Cited by 60 publications

References 44 publications

Carcinogenesis: Failure of resolution of inflammation?

Carcinogenesis: Failure of resolution of inflammation?

Current perspectives on the immunosuppressive tumor microenvironment in hepatocellular carcinoma: challenges and opportunities

Identifying cancer-associated fibroblasts as emerging targets for hepatocellular carcinoma

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