Hepatocyte growth factor activates tumor stromal fibroblasts to promote tumorigenesis in gastric cancer

Xin, Wu; Chen, Xuehua; Zhou, Quan; Li, Pu; Yu, Beiqin; Li, Jianfang; Qu, Ying; Yan, Jun; Yu, Yingyan; Yan, Min; Zhu, Zhenggang; Liu, Bingya; Su, Liping

doi:10.1016/j.canlet.2013.02.002

Cited by 84 publications

(70 citation statements)

References 34 publications

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“…Moreover, TGF-b and FGF-7 produced from fibroblasts could increase scirrhous gastric cancer cell proliferation and invasiveness [42]. Wu et al [44] also demonstrated that HGF is an important factor secreted from CAFs that could accelerate tumorigenesis in gastric cancer in a paracrine manner. Furthermore, PTEN signaling is also closely associated with growth factors and chemokines from CAFs.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐106b in cancer‐associated fibroblasts from gastric cancer promotes cell migration and invasion by targeting PTEN

Yang

Chen

et al. 2014

FEBS Letters

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Edited by Varda Rotter Keywords:Cancer associated fibroblasts microRNA Protein tyrosine phosphatase and tensin homologue Gastric cancer a b s t r a c t It is well established that the interaction between cancer cells and microenvironment has a critical role in tumor development, but the roles of miRNAs in this interaction are rarely known. Here, we have shown that miR-106b is up-regulated in cancer associated fibroblasts compared with normal fibroblasts established from patients with gastric cancer, the expression level of miR-106b is associated with poor prognosis of patients, and CAFs with down-regulated miR-106b could significantly inhibit gastric cancer cell migration and invasion by targeting PTEN. Taken together, these data suggest that miR-106b might be a novel candidate target for the treatment of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐106b in cancer‐associated fibroblasts from gastric cancer promotes cell migration and invasion by targeting PTEN

Yang

Chen

et al. 2014

FEBS Letters

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Section: Promotion Of Metastasis By Cafmentioning

confidence: 99%

“…The CAFs in gastric cancer have high expression levels of HGF and are one of the sources of secreted HGF in the microenvironment (62). HGF enhances the proliferation and migration of gastric cancer cells via paracrine signalling (62). A number of ECM proteins secreted from CAFs also have a role in the promotion of gastric cancer, including asporin and periostin (63,64).…”

Section: Promotion Of Metastasis By Cafmentioning

confidence: 99%

Mechanisms of peritoneal dissemination in gastric cancer (Review)

2017

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Abstract. Peritoneal dissemination is the most frequent metastatic pattern of gastric cancer, but the mechanisms underlying peritoneal dissemination are yet to be elucidated. Paget's 'seed and soil' hypothesis is recognized as the fundamental theory of metastasis. The 'seeding' theory proposes that the formation of peritoneal dissemination is a multistep process, including detachment from the primary tumour, transmigration and attachment to the distant peritoneum, invasion into subperitoneal tissue and proliferation with blood vascular neogenesis. In the present review, the progress of each step is discussed. Milky spots, as a lymphatic apparatus, are indicative of lymphatic orifices on the surface of the peritoneum. These stomata are open gates for peritoneal-free cancer cells to migrate into the submesothelial space. Therefore, milky spots provide suitable 'soil' for cancer cells to implant. Other theories have also been proposed to clarify the peritoneal dissemination process, including the transvessel metastasis theory, which suggests that the peritoneal metastasis of gastric cancer develops via a vascular network mediated by hypoxia inducible factor-1α.

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“…Candidate genes in this region with a possible role in PanNET pathogenesis and progression include CD36 as a prominent adhesion molecule and hepatocyte growth factor, a regulatory protein implicated in cell growth, proliferation, motility and matrix invasion rendering it a central element in tumorogenesis and tumor dissemination [22,23] . The 8q24.3 locus was altered in approximately 20% of both primary tumor samples and metastases.…”

Section: Discussionmentioning

confidence: 99%

Genomic landscape of pancreatic neuroendocrine tumors

Gebauer

Schmidt-Werthern

Bernard

et al. 2015

Exp Clin Endocrinol Diabetes

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AIM:To investigate the prognostic role of genomic stability and copy number alterations (CNAs) pancreatic neuroendocrine tumors (PanNETs). METHODS:A high-resolution array-based comparative genomic hybridization approach was utilized in order to investigate and quantify chromosomal aberrations in a panel of 37 primary PanNET and 11 metastatic samples. DNA samples were extracted from formalinfixed and paraffin-embedded tumor specimen. Genomic findings were correlated with histopathological and immunohistochemical data. Moreover, the dataset was subjected to employing an unsupervised hierarchical clustering analysis approach utilizing Euclidean distance and average linkage and associations between genomically defined tumor groups and recurrent CNAs or clinicopathological features of the study group were assessed. RESULTS:Numerous chromosomal aberrations were recurrently detected in both, primary tumor samples and metastases. Copy number gains were most frequently observed at 06p22.2-p22.1 (27.1%), 17p13.1 (20.8%), 07p21.3-p21.2 (18.8%), 09q34.11 (18.8%). Genomic losses were significantly less frequent and the only recurrent aberration affected 08q24.3 (6.3%). Moreover, we detected a high degree of genomic heterogeneity between primary tumors and metastatic lesions. Unsupervised hierarchical clustering of loci affected by CNAs in more than 3 primary tumor samples revealed two genetically distinct tumor groups as well as two chromosomal clusters of genomic imbalances indicating a small subset of tumors with common molecular features (13.5%). Aberrations affecting 6p22.2-22.1, 8q24.3, 9q34.11 and 17p13.1 (P = 0.011; 0.003; 0.003; 0.001), were significantly associated with a poorer survival prognosis. CONCLUSION:This study suggests that several frequent CNAs in numerous candidate regions are involved in the pathogenesis and metastatic progression of Pan-NET. Gebauer N et al . Chromosomal aberrations in PanNETs (PanNETs). Analysis of recurrent genomic amplifications delineated two independent clusters of genomic aberrations as well as two patient groups characterized by significantly overlapping cytogenetic features. Copy number alterations affecting chromosomes 6, 8, 9 and 17 were shown to be associated with survival. A high degree of genomic heterogeneity between primary tumor samples and metastatic lesions demonstrates the need for a more focused molecular and cytogenetic characterization in the light of upcoming targeted therapy approaches. PanNETs appear to be genetically distinct from other types of neuroendocrine tumors.

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Hepatocyte growth factor activates tumor stromal fibroblasts to promote tumorigenesis in gastric cancer

Cited by 84 publications

References 34 publications

MicroRNA‐106b in cancer‐associated fibroblasts from gastric cancer promotes cell migration and invasion by targeting PTEN

MicroRNA‐106b in cancer‐associated fibroblasts from gastric cancer promotes cell migration and invasion by targeting PTEN

Mechanisms of peritoneal dissemination in gastric cancer (Review)

Genomic landscape of pancreatic neuroendocrine tumors

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