Vascular Changes in Hepatocellular Carcinoma

Yang, Zhen; Poon, Ronnie Tung Ping

doi:10.1002/ar.20668

Cited by 183 publications

(179 citation statements)

References 154 publications

(156 reference statements)

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“…Angiogenesis has an important role in its development, progression and metastasis (Yang and Poon, 2008). As PEDF is a potent inhibitor of angiogenesis, the study sought to determine whether delivery of hMSCs-PEDF reduces intratumoral angiogenesis.…”

Section: Therapeutic Effects Of Hmscs-pedf On Hcc In Vivomentioning

confidence: 99%

“…Angiogenesis, the process by which new blood vessels develop from preexisting blood vessels, is an essential step that enables tumors to gain their own sustainable blood supply, therefore supporting further growth and metastasis (Chen et al, 2001;Persano et al, 2007). Hence, angiogenesis inhibitors, targeting either the neovasculature or the signals that promote new vessel growth should be a promising approach in the treatment of HCC, now that it is known to be one of the most vascular solid tumors (Yang and Poon, 2008). Pigment epithelial-derived factor (PEDF) is a 50-kDa secreted glycoprotein, which was initially identified as a neurotrophic factor (Tombran-Tink and Johnson, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Human mesenchymal stem cells overexpressing pigment epithelium-derived factor inhibit hepatocellular carcinoma in nude mice

et al. 2010

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The poor outcome of cancer gene therapy in clinical trials relates in part to insufficient gene delivery to tumor sites. Mesenchymal stem cells (MSCs) represent a new tool for the delivery of therapeutic agents to tumor cells. This study used an orthotopic nude mice model of hepatocellular carcinoma (HCC) to evaluate the potential of genetically modified human MSCs (hMSCs), to function as an effective delivery vehicle for therapeutic genes. hMSCs derived from the bone marrow were efficiently engineered to express human pigment epithelium-derived factor (PEDF) by lentiviral transduction, then tested in vitro for high-level expression and bioactivity of the transgenic protein. The preferential homing of hMSCs toward HCC was confirmed by in vitro and in vivo migration assays. in vivo efficacy experiments showed that intravenous (i.v.) injection of PEDF-expressing hMSCs significantly suppressed both the growth of primary liver tumors and the development of pulmonary metastases. Moreover, hMSCs-based PEDF gene delivery moderately increased the systemic levels of human PEDF. Immunohistochemistry of primary liver tumors demonstrated lower microvessel density in mice treated with hMSCs-PEDF than in control mice. This is the first study to show the potential of hMSCs as an effective delivery vehicle for therapeutic genes in the treatment of HCC.

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Section: Therapeutic Effects Of Hmscs-pedf On Hcc In Vivomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human mesenchymal stem cells overexpressing pigment epithelium-derived factor inhibit hepatocellular carcinoma in nude mice

et al. 2010

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“…As one of the most vascularized solid tumors, the HCC progression and prognosis correlate with the status of angiogenesis, 10 due largely to elevated production of angiogenic factors, such as interleukin-8 (IL-8, CXCL8) by tumor cells. 11 Previous reports have implicated IL-8 in the growth and angiogenesis of malignant tumors.…”

mentioning

confidence: 99%

Formylpeptide receptor 1 mediates the tumorigenicity of human hepatocellular carcinoma cells

et al. 2015

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G protein-coupled chemoattractant receptors (GPCRs) have been implicated in cancer progression. Formylpeptide receptor 1 (FPR1) was originally identified as a GPCR mediating anti-microbial host defense. However, the role of FPR1 in tumorigenesis remains poorly understood. The current study aims to investigate the potential of FPR1 to regulate human hepatoma growth and invasion. We found the FPR1 gene and protein expression in human intratumoral and peritumoral tissues of hepatocellular carcinoma (HCC) specimens and in human hepatoma cell lines. FPR1 activation mediated the migration, calcium mobilization and ERK-dependent IL-8 production by hepatic cancer cells. FPR1 knockdown substantially reduced the tumorigenicity of hepatoma cells in nude mice. Necrotic hepatic tumor cells released factor(s) that activated FPR1 in live tumor cells. Our results indicate a critical role of FPR1 in the progression of malignant human hepatic cancer. FPR1 thus may represent a molecular target for the development of novel anti-hepatoma therapeutics.

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“…Hepatic sinusoidal capillarization is a basic pathological change associated with hepatic fibrosis and cirrhosis (10)(11)(12)(13). Hepatic sinusoidal capillarization plays a key role in the pathogenesis and progression of this process, and it can also induce hepatocellular carcinoma along with a newly forming arterial blood supply (14)(15)(16). Defenestration of LSECs, a typical phenomenon that occurs during hepatic sinusoidal capillarization, plays a unique role in liver fibrosis and cirrhosis.…”

Section: Introductionmentioning

confidence: 99%