Tumour-microenvironmental interactions: paths to progression and targets for treatment

Box, Carol; Rogers, Susanne; Mendiola, Marta; Eccles, Suzanne A.

doi:10.1016/j.semcancer.2010.06.004

Cited by 88 publications

(50 citation statements)

References 149 publications

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“…The microenvironment of the tumor is widely known to be an important regulator in cancer development (2,3,19). Tumor cells consistently release immunosuppressive and proinflammatory factors that facilitate tumor immune-escape and tumor progression (20,21).…”

Section: Discussionmentioning

confidence: 99%

Lung Cancer-derived Galectin-1 Enhances Tumorigenic Potentiation of Tumor-associated Dendritic Cells by Expressing Heparin-binding EGF-like Growth Factor

Kuo

Huang

Cheng

et al. 2012

Journal of Biological Chemistry

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Background: Communication between cancer cells and immune cells in their microenvironment leads to cancer progression. Results: Lung cancer-derived galectin-1 stimulates HB-EGF expression and triggers a release mechanism in tumor-associated dendritic cells that stimulates tumor cell growth and invasion. Conclusion: The galectin-1/HB-EGF cycle between cancer and dendritic cells enhances lung cancer progression. Significance: Galectin-1 is a potential therapeutic target for inhibiting tumor-promoting immune cells in the tumor microenvironment.

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Section: Discussionmentioning

confidence: 99%

Lung Cancer-derived Galectin-1 Enhances Tumorigenic Potentiation of Tumor-associated Dendritic Cells by Expressing Heparin-binding EGF-like Growth Factor

Kuo

Huang

Cheng

et al. 2012

Journal of Biological Chemistry

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“…Overexpression of EGFR and TGFα significantly predicted a shorter disease-free and overall survival (9). EGFR activation also resulted into increased cell invasiveness and motility (10) via the induction of epithelial-to-mesenchymal transition (11,12). Furthermore, EGFR can interact with the receptor cluster of differentiation 44, resulting in a migratory cell phenotype (13 (16,17).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of EGFR as a prognostic and diagnostic marker for head and neck squamous cell carcinoma patients

et al. 2016

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Abstract. Approximately 90% of all head and neck tumors are squamous cell carcinomas. The overall survival of patients with head and neck squamous cell carcinoma (HNSCC) is low (≤50%). A non-invasive marker of disease progression is sorely required. The present study focused on the plasmatic levels of epidermal growth factor receptor (EGFR) in HNSCC patients (N=92) compared with healthy (N=29) and diabetic [type 2 diabetes mellitus (T2DM); N=26] controls. Enzymelinked immunosorbent assay using antibodies against the extracellular region of EGFR (L25-S645) was performed. No significant changes were observed between diabetic and healthy controls. However, there were significantly higher EGFR plasma levels in HNSCC patients compared with both control groups (P=0.001 and 0.005, respectively). Receiver operating characteristic curve analysis identified a sensitivity of 76.09%, a specificity of 67.27% and an area under curve of 0.727 for this comparison. No significant association was observed between EGFR plasma levels and tumor stage, tumor grade, lymph node or distant metastasis occurrence, smoking habit or hypertension. However, the presence of human papillomavirus infection and T2DM in HNSCC patients had borderline effect on the plasma EGFR levels. Survival analysis revealed no significant influence of plasmatic EGFR levels on the overall and disease-specific survival of HNSCC patients. In conclusion, EGFR plasma levels appear to be a relatively promising diagnostic, but poor prognostic, HNSCC marker.

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“…In this regard, we hypothesize that the limitation of tumor cell migration by EMMPRIN leads to the activation of cell-cell interaction between the tumor and adjacent stroma cells, which progresses the degradation of peritumoral extracellular matrix (ECM) due to the augmentation of MMP production. Thereafter, the alteration of peritumoral ECM may trigger the dissociation of cell-ECM interaction and the heterophilic dimerization of EMMPRIN through adhesion molecules such as integrins, which in turn facilitate the dissemination, migration, and invasion of tumor cells in vivo (29,30). This hypothesis can be supported by previous reports that: i) the integrin-dependent signal stimulates the malignant transformation and invasive phenotype in human cervical carcinoma (31,32), and ii) EMMPRIN binds to integrin α3β1 and α6β1 in some tumor cell lines (33)(34)(35).…”

mentioning

confidence: 99%

A novel functional site of extracellular matrix metalloproteinase inducer (EMMPRIN) that limits the migration of human uterine cervical carcinoma cells

Sato

Watanabe²,

Hashimoto³

et al. 2011

Int J Oncol

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Abstract. EMMPRIN (extracellular matrix metalloproteinase inducer)/CD147, a membrane-bound glycoprotein with two extracellular loop domains (termed loops I and II), progresses tumor invasion and metastasis by increasing the production of matrix metalloproteinase (MMP) in peritumoral stoma cells. EMMPRIN has also been associated with the control of migration activity in some tumor cells, but little is known about how EMMPRIN regulates tumor cell migration. In the present study, EMMPRIN siRNA suppressed the gene expression and production of EMMPRIN in human uterine cervical carcinoma SKG-II cells. An in vitro scratch wound assay showed enhancement of migration of EMMPRIN-knockdown SKG-II cells. In addition, the SKG-II cell migration was augmented by adding an E. coli-expressed human EMMPRIN mutant with two extracellular loop domains (eEMP-I/II), which bound to the cell surface of SKG-II cells. However, eEMP-I/II suppressed the native EMMPRIN-mediated augmentation of proMMP-1/procollagenase-1 production in a co-culture of the SKG-II cells and human uterine cervical fibroblasts, indicating that the augmentation of SKG-II cell migration resulted from the interference of native EMMPRIN functions by eEMP-I/ II on the cell surface. Furthermore, a systematic peptide screening method using nine synthetic EMMPRIN peptides coding the loop I and II domains (termed EM1-9) revealed that EM9 ( 170 HIENLNMEADPGQYR 184 ) facilitated SKG-II cell migration. Moreover, SKG-II cell migration was enhanced by administration of an antibody against EM9, but not EM1 which is a crucial site for the MMP inducible activity of EMMPRIN. Therefore, these results provide novel evidence that EMMPRIN on the cell surface limits the cell migration of human uterine cervical carcinoma cells through 170 HIENLNMEADPGQYR 184 in the loop II domain. Finally, these results should provide an increased understanding of the functions of EMMPRIN in malignant cervical carcinoma cells, and could contribute to the development of clinical strategies for cervical cancer therapy.

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Tumour-microenvironmental interactions: paths to progression and targets for treatment

Cited by 88 publications

References 149 publications

Lung Cancer-derived Galectin-1 Enhances Tumorigenic Potentiation of Tumor-associated Dendritic Cells by Expressing Heparin-binding EGF-like Growth Factor

Lung Cancer-derived Galectin-1 Enhances Tumorigenic Potentiation of Tumor-associated Dendritic Cells by Expressing Heparin-binding EGF-like Growth Factor

Evaluation of EGFR as a prognostic and diagnostic marker for head and neck squamous cell carcinoma patients

A novel functional site of extracellular matrix metalloproteinase inducer (EMMPRIN) that limits the migration of human uterine cervical carcinoma cells

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