Experimental anti‐angiogenesis causes upregulation of genes associated with poor survival in glioblastoma

Saidi, Ahlame; Javerzat, Sophie; Bellahcène, Akeila; Vos, John De; Bello, Lorenzo; Castronovo, Vincenzo; Deprez, Manuel; Loiseau, Hugues; Bikfalvi, Andréas; Hagedorn, Martin

doi:10.1002/ijc.23313

Cited by 101 publications

(85 citation statements)

References 45 publications

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“…If the oxygen supply is insufficient, the resulting hypoxia stimulates angiogenesis through upregulation of HIF-1α and VEGF (Hendriksen et al, 2009). VEGF upregulation is associated with a poor response to treatment and poor prognosis (Saidi et al, 2008). In our study, we demonstrate that there was only DOI:http://dx.doi.org/10.7314/APJCP.2012.13.8.3675 Expression of Endogenous Hypoxia Markers in Vulvar Squamous Cell Carcinoma 25% of control sections with weak VEGF expression, while strong staining was found in about 60% of VIN sections and 25% of VSCC sections.…”

Section: Discussionmentioning

confidence: 54%

Expression of Endogenous Hypoxia Markers in Vulvar Squamous Cell Carcinoma

Li²,

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Objective: To investigate the expression of endogenous hypoxia-related markers identified as being involved in vulvar squamous cell carcinoma (VSCC). Methods: We performed immunohistochemical staining of hypoxia-inducible factor-1α (HIF-1α), glucose transporter-1 (GLUT-1), carbonic anhydrase 9 (CA-9) and vascular endothelial growth factor (VEGF), on tissue sections of 25 VSCC patients, 10 vulvar intraepithelial neoplasia (VIN) patients and 12 healthy controls. Results: HIF-1α expression was found in all sections, with no significant difference between controls, VIN and VSCC sections (all P<0.05). Glut-1 expression was found in 25% of control, 90% of VIN and 100% of VSCC sections. A significant difference between control and VIN or VSCC was observed (all P<0.05), while no difference was found between VIN and VSCC sections (P>0.05). CA-9 expression was negative in control sections, but it was found in 30% of VIN sections and 52% of VSCC sections with strong staining. Similarly, CA-9 expression also showed obvious differences between controls and VIN or VSCC sections (all P<0.05). However, there was no significant difference between VIN and VSCC (P>0.05). There were only 25% of control sections with weak VEGF expression, while strong staining was found in about 60% of VIN sections and 25% of VSCC sections (all P<0.05). In addition, a difference was also found between VIN and VSCC sections (P<0.05). Conclusion: Expression of endogenous hypoxia markers (HIF-1α, GLUT-1, CA-9 and VEGF) might be involved in the malignant progression of VSCC.

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Section: Discussionmentioning

confidence: 54%

Expression of Endogenous Hypoxia Markers in Vulvar Squamous Cell Carcinoma

Li²,

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…30 Sections of 10 mm were stained with haematoxylin and eosin. For immunohistology studies, the following primary antibodies were used: Ab-2 (clone V9, NeoMarkers Ab, Montluc¸on, France) for vimentin, Anti Ki-67 (AnaSpec Inc., Fremont, CA, USA) for Ki-67, fluorescein-coupled SNA-1 (AbCys, Paris, France) for SNA-lectin.…”

Section: Histology and Immunochemistrymentioning

confidence: 99%

The p53 isoform, Δ133p53α, stimulates angiogenesis and tumour progression

et al. 2012

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The tumour suppressor p53, involved in DNA repair, cell cycle arrest and apoptosis, also inhibits blood vessel formation, that is, angiogenesis, a process strongly contributing to tumour development. The p53 gene expresses 12 different proteins (isoforms), including TAp53 (p53 (or p53a), p53b and p53g) and D133p53 isoforms (D133p53a, D133p53b and D133p53g). The D133p53a isoform was shown to modulate p53 transcriptional activity and is overexpressed in various human tumours. However, its role in tumour progression is still unexplored. In the present study, we examined the involvement of D133p53 isoforms in tumoural angiogenesis and tumour growth in the highly angiogenic human glioblastoma U87. Our data show that conditioned media from U87 cells depleted for D133p53 isoforms block endothelial cell migration and tubulogenesis without affecting endothelial cell proliferation in vitro. The D133p53 depletion in U2OS osteosarcoma cells resulted in a similar angiogenesis blockade. Furthermore, using conditioned media from U87 cells ectopically expressing each D133p53 isoform, we determined that D133p53a and D133p53g but not D133p53b, stimulate angiogenesis. Our in vivo data using the chicken chorio-allantoic membrane and mice xenografts establish that angiogenesis and growth of glioblastoma U87 tumours are inhibited upon depletion of D133p53 isoforms. By TaqMan low-density array, we show that alteration of expression ratio of D133p53 and TAp53 isoforms differentially regulates angiogenic gene expression with D133p53 isoforms inducing pro-angiogenic gene expression and repressing anti-angiogenic gene expression.

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“…Brain [74,[123][124][125][126][127][128][129][130][131][132] Squamous cell carcinoma of the head and neck…”

Section: Glioma Oligodendroglioma Glioblastomamentioning

confidence: 99%

Potential role of chitinase 3-like-1 in inﬂammationassociated carcinogenic changes of epithelial cells

Eurich¹,

Segawa²,

Toei-Shimizu³

et al. 2009

WJG

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The family of mammalian chitinases includes members both with and without glycohydrolase enzymatic activity against chitin, a polymer of N-acetylglucosamine. Chitin is the structural component of fungi, crustaceans, insects and parasitic nematodes, but is completely absent in mammals. Exposure to antigens containing chitin-or chitin-like structures sometimes induces strong T helper type-I responses in mammals, which may be associated with the induction of mammalian chitinases. Chitinase 3-like-1 (CHI3L1), a member of the mammalian chitinase family, is induced specifically during the course of inflammation in such disorders as inflammatory bowel disease, hepatitis and asthma. In addition, CHI3L1 is expressed and secreted by several types of solid tumors including glioblastoma, colon cancer, breast cancer and malignant melanoma. Although the exact function of CHI3L1 in inflammation and cancer is still largely unknown, CHI3L1 plays a pivotal role in exacerbating the inflammatory processes and in promoting angiogenesis and remodeling of the extracellular matrix. CHI3L1 may be highly involved in the chronic engagement of inflammation which potentiates development of epithelial tumorigenesis presumably by activating the mitogen-activated protein kinase and the protein kinase B signaling pathways. Anti-CHI3L1 antibodies or pan-chitinase inhibitors may have the potential to suppress CHI3L1-mediated chronic inflammation and the subsequent carcinogenic change in epithelial cells.

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Experimental anti‐angiogenesis causes upregulation of genes associated with poor survival in glioblastoma

Cited by 101 publications

References 45 publications

Expression of Endogenous Hypoxia Markers in Vulvar Squamous Cell Carcinoma

Expression of Endogenous Hypoxia Markers in Vulvar Squamous Cell Carcinoma

The p53 isoform, Δ133p53α, stimulates angiogenesis and tumour progression

Potential role of chitinase 3-like-1 in inﬂammationassociated carcinogenic changes of epithelial cells

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