Disease relevance of C11orf2

• A novel gene, C11orf2, was identified by BLAST search in the human chromosome 11p15.5 region potentially responsible for Beckwith-Wiedemann Syndrome (BWS) and some cancers [1].
• In this study, we determined Ang2 mRNA expression in cultured human malignant glioma cells (U105, U251, and U373 MG) by reverse transcriptase-PCR [2].
• Furthermore, hypoxia increased the Ang2 protein level in cultured glioma cells [2].
• Hepatic expression of ANG2 RNA in metastatic colorectal cancer [3].
• Ang2 protein was detected not only in endothelial cells but also in glioma cells, and its expression was prominent in both the area surrounding the necrosis and the periphery of glioblastomas [2].

High impact information on C11orf2

• Furthermore, combination of Ang1/Ang2 induced an additive effect on neutrophil adhesion but not on P-selectin translocation [4].
• RESULTS: Univariate analysis of overall survival indicated the following variables as prognostic factors: good response on a day-15 bone marrow examination after initiation of induction chemotherapy, karyotype, and high Ang2 expression [5].
• The increase in ANG2 RNA content from the peripheral portion of the tumor to the intermediate portion, coinciding with the decrease in recruitment of periendothelial supporting cells around the vascular endothelial cells, suggests that Ang-2 may play a role in the immaturity of tumor vessels [3].
• Reverse-transcription polymerase chain reaction assays indicated that the ANG2 RNA content was greater in metastatic CRC than in primary CRC [3].
• In the tumor periphery, Ang2 was highly expressed and many small vessels stained positively for von Willebrand factor but not for alpha smooth muscle actin, suggesting angiogenesis [2].

Biological context of C11orf2

• Here, we found that a high concentration of Ang2 (800 ng/ml) acts as an apoptosis survival factor for endothelial cells during serum deprivation apoptosis [6].
• Ang2 mRNA was 400- and 100-fold higher than Ang1 and VEGF-A, respectively, in the first trimester and declined to 20-fold and 7-fold in the third [7].
• Northern blot analysis was performed to examine the time course and dose response of Ang1 and Ang2 mRNA expression. mRNA stability and nuclear run-on analyses were performed [8].
• The gene expression levels of Ang2 and Tie2 were statistically the same in both groups [9].
• Furthermore, cellular distribution of Ang1 and Ang2 mRNA was examined by in situ hybridization, and localization of Tie2 was studied by immunochemistry [9].

Anatomical context of C11orf2

• METHODS AND RESULTS: In normal renal tissue, the expression of ANG-1 was apparent in the glomerular capillaries and podocytes as well as in the endothelial cells of vessels, whereas we observed no expression of ANG-2 [10].
• Intense ANG-2 expression was observed in the cancer cells themselves as well as in the endothelial cells, where its expression was restricted to small vessels or neoplastic capillaries and not mature vessels [10].
• Immunohistochemical study demonstrated marked production of ANG-1 in fibroblasts and ANG-2 expression in cancer cells when we performed co-culture, but no expression of either in each monoculture [10].
• Using the polymerase chain reaction, we isolated a cDNA encoding a novel shorter form of Ang2 from human umbilical vein endothelial cell cDNA and have designated it angiopoietin-2(443) (Ang2(443)), because it contains 443 amino acids [11].
• Macrophages express mainly Ang2 mRNA, but the expression of Ang2(443) mRNA is temporarily up-regulated during macrophage differentiation [11].

Associations of C11orf2 with chemical compounds

• The survival effect of high concentration Ang2 was blocked by pre-treatment with soluble Tie2 receptor and the PI 3'-kinase-specific inhibitors, wortmannin and LY294002 [6].
• In ZR75.1 and T47D cells, expression of ANG2 mRNA was increased up to 10-fold by treatment with estrogen within 24 hr [12].
• Ang1 and Ang2 bind with similar affinity to the endothelial cell tyrosine kinase receptor Tie2 [9].
• Differential regulation of ANG2 and VEGF-A in human granulosa lutein cells by choriogonadotropin [13].

Analytical, diagnostic and therapeutic context of C11orf2

• Western blot analysis and immunocytochemical analysis with antihuman Ang2 antibody revealed that Ang2 protein was expressed and secreted by these cells [2].
• Quantitative real-time PCR analysis demonstrated that VEGF-A and Ang1 mRNA increased in a linear pattern by 2.5 (not significant) and 2.8%/wk (P = 0.034), respectively, whereas Ang2 decreased logarithmically by 3.5%/wk (P = 0.0003) [7].
• Total RNA from biopsies of 38 breast cancer patients was extracted and ANG1 and ANG2 mRNA expression was measured by means of quantitative real-time RT-PCR (Taqman) [12].

References