Direct Interaction between Carcinoma Cells and Cancer Associated Fibroblasts for the Regulation of Cancer Invasion

Yamaguchi, Hideki; Sakai, Ryuichi

doi:10.3390/cancers7040876

Cited by 107 publications

(100 citation statements)

References 59 publications

(64 reference statements)

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“…The CAFs were shown to mediate cancer‐related inflammation by expressing proinflammatory and tumor‐promoting factors and promotion of the cancer cell invasion and ECM remodeling 30, 31. Moreover, under the control of a variety of stroma‐modulating factors, the cancer cells themselves generate a permissive microenvironment favoring further tumor development and invasion 32, 33, 34…”

Section: Introductionmentioning

confidence: 99%

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

et al. 2018

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BackgroundMajor human gastrointestinal pathogen Helicobacter pylori (H. pylori) colonizes the gastric mucosa causing inflammation and severe complications including cancer, but the involvement of fibroblasts in the pathogenesis of these disorders in H. pylori‐infected stomach has been little studied. Normal stroma contains few fibroblasts, especially myofibroblasts. Their number rapidly increases in the reactive stroma surrounding inflammatory region and neoplastic tissue; however, the interaction between H. pylori and fibroblasts remains unknown. We determined the effect of coincubation of normal rat gastric fibroblasts with alive H. pylori (cagA+vacA+) and H. pylori (cagA−vacA−) strains on the differentiation of these fibroblasts into cells possessing characteristics of cancer‐associated fibroblasts (CAFs) able to induce epithelial‐mesenchymal transition (EMT) of normal rat gastric epithelial cells (RGM‐1).Materials and MethodsThe panel of CAFs markers mRNA was analyzed in H. pylori (cagA+vacA+)‐infected fibroblasts by RT‐PCR. After insert coculture of differentiated fibroblasts with RGM‐1 cells from 24 up to 48, 72, and 96 hours, the mRNA expression for EMT‐associated genes was analyzed by RT‐PCR.ResultsThe mRNA expression for CAFs markers was significantly increased after 72 hours of infection with H. pylori (cagA+vacA+) but not H. pylori (cagA−vacA−) strain. Following coculture with CAFs, RGM‐1 cells showed significant decrease in E‐cadherin mRNA, and the parallel increase in the expression of Twist and Snail transcription factors mRNA was observed along with the overexpression of mRNAs for TGFβR, HGFR, FGFR, N‐cadherin, vimentin, α‐SMA, VEGF, and integrin‐β1.Conclusion Helicobacter pylori (cagA+vacA+) strain induces differentiation of normal fibroblasts into CAFs, likely to initiate the EMT process in RGM‐1 epithelial cell line.

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Section: Introductionmentioning

confidence: 99%

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

et al. 2018

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“…Activated fibroblasts, termed cancer‐associated fibroblasts (CAFs), are one of the major components of stromal cells. CAFs, play an important role in promoting cancer initiation, growth, invasion, metastasis, therapeutic resistance, angiogenesis, and remodeling of the extracellular matrix . Thus, it is necessary to identify novel markers of CAFs that represent an effective therapeutic target for cancer.…”

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confidence: 99%

The role of Tenascin‐C and Twist1 in gastric cancer: cancer progression and prognosis

Yang

et al. 2019

APMIS

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The aim of the present study was to identify the relation between Tenascin‐C (TNC) and Twist1 and determine their clinical significance in gastric cancer (GC). We analyzed the expression of TNC and Twist1 in 159 GC samples and in 91 non‐tumor samples using immunohistochemistry. In this study, TNC expression in stromal fibroblasts of GC was remarkably higher than non‐tumor gastric lesions. The expression of TNC in GC stromal fibroblasts was significantly associated with pT stage, lymph node metastasis, distant metastasis. Twist1 expression in stromal fibroblasts of GC was remarkably higher than non‐tumor gastric lesions. Twist1 expression in the stromal fibroblasts of GC was associated with tumor size, lymph node metastasis, and clinical stage. Furthermore, TNC expression levels in GC stromal fibroblasts were positively associated with Twist1. The simultaneous expression of TNC and Twist1 was significantly higher in stromal fibroblasts of GC than in noncancerous tissues. The simultaneous expression of TNC and Twist1 in GC stromal fibroblasts was positively associated with tumor location, pT stage, lymph node metastasis and clinical stage. Moreover, patients with co‐expression of TNC and Twist1 had a poorer prognosis than either TNC or Twist1 positive in GC. Our study revealed that the simultaneous expression of TNC and Twist1 indicated the poorer prognosis of GC. Co‐targeting TNC and Twist1 confer significant clinical advantage, which offers a novel therapeutic target in GC.

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“…Examination of genetic background and intercellular signaling may unveil regulatory biomarkers that regard GOQ-2 and GOQ-3. Tumor invasion is variably dynamic and thought to occur by EMT processes in some contexts [204,[219][220][221][222][223]. However, the EMT is not the only program for tumor invasion.…”

Section: Molecular Connections Between Lc and Pcmentioning

confidence: 99%

“…The Hh pathway also plays a role in driving forward hypoxia-induced EMT processes [242]. Hypoxia and metabolic stress (nutrient deprivation) induce the stem cell niche to initiate tumor invasion and drug resistance through tumor-stromal paracrine signaling [110,159,220,237,241,[243][244][245].…”

Section: Molecular Connections Between Lc and Pcmentioning

confidence: 99%

The Molecular Connections between Lung and Pancreatic Cancer Metastases: are we not seeing the Forest for the Trees?

Wilson¹

2017

JCPCR

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Metastases to the pancreas are rare at 1-2%. Among primaries metastasizing to the pancreas, lung cancer (LC) is frequently the culprit. Metastases to the lung from pancreatic cancer (PC) are significantly more common at about 45%, presenting striking differences in cancer behavior. There are conflicting reports regarding cancerogenicity and metastatic incidence between the lung and pancreas. Therefore, this review takes a fresh look at lung and pancreatic cancer behavior. Secondary metastases to the lung and pancreas are often indistinguishable from LC and PC primaries, and the seed and soil hypothesis is not always congruous with clinical interpretation of disease course. Sometimes single "seed" dissemination is thought to occur at the preneoplastic stage without any evidence of tumor invasion. Metastatic growth may become dormant, manifesting years later as cancer of unknown primary (CUP). Interestingly, CUPs are discovered to originate most frequently from LC and PC primaries at autopsy. The lung and pancreas are morphologically related through endoderm-level morphogenesis. The molecular basis of cancer regularity between them involves developmental signaling pathways including HEDGEHOG, NOTCH, WNT, and CXCL12/CXCR4, an evolving genetic background, and regulatory tumor-stromal interactions. Perhaps biomarkers that explain the regularity between them have been documented -as we peruse the bioscience literature for information, we may be reading through viable biomarkers and solutions and not seeing the forest for the trees. On the other hand, perhaps more research is warranted to explain cancer behavior between the lung and pancreas. Observations in this review provide a framework on which to extract clues for future work regarding organspecific metastasis between the lung and pancreas.

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Direct Interaction between Carcinoma Cells and Cancer Associated Fibroblasts for the Regulation of Cancer Invasion

Cited by 107 publications

References 59 publications

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

The role of Tenascin‐C and Twist1 in gastric cancer: cancer progression and prognosis

The Molecular Connections between Lung and Pancreatic Cancer Metastases: are we not seeing the Forest for the Trees?

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