Dataset Information

Analysis of expression levels of markers associated with tumor proliferation and angiogenesis in familial adenomatous polyposis.

ABSTRACT:

Background

Familial adenomatous polyposis (FAP) is an autosomal dominant hereditary disease with colorectal adenomatous polyps as the main clinical manifestations. The objective of this study was to analyze and compare the expression levels of tumor proliferation and angiogenesis-related genes in different tissue sections of FAP patients through qPCR, western blot, and immunohistochemistry (IHC) analysis.

Methods

Seventeen patients with FAP admitted to Tianjin Union Medical Center from January 2010 to June 2015 were selected, and then, normal intestinal mucosa, polyp tissue, or cancerous polyp tissue were collected. QPCR, western blot, and IHC were used to detect the expression level of genes or proteins correlated with tumor proliferation.

Results

The mRNA expression of CD31 in large polyp tissue was significantly higher than that in normal tissue and small polyp tissue. Compared with normal tissue and polyp tissue, the expression level of KI67 mRNA in cancer tissue was remarkably increased. The VEGFA mRNA and CDH5 mRNA expression in both polyp and cancer tissues were prominently lower than those in normal tissue. The expression of CD31 protein in cancer tissue was lower than that in normal tissue and polyp tissue, whereas the expression levels of VEGF, CDH5, and KI67 protein were widely higher than that in normal tissue and polyp tissue.

Conclusion

Abnormal expressions of CD31, KI67, VEGF(A), and CDH5 were associated with the carcinogenesis of FAP.

SUBMITTER: Zhang Z

PROVIDER: S-EPMC7767556 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Analysis of expression levels of markers associated with tumor proliferation and angiogenesis in familial adenomatous polyposis.

Zhang Zhao Z Wang Dan D Xu Chen C Li Yuwei Y Yu Yongjun Y Chen Chao C Li Mingsen M Zhang Xipeng X

Molecular genetics & genomic medicine 20201027 12

<h4>Background</h4>Familial adenomatous polyposis (FAP) is an autosomal dominant hereditary disease with colorectal adenomatous polyps as the main clinical manifestations. The objective of this study was to analyze and compare the expression levels of tumor proliferation and angiogenesis-related genes in different tissue sections of FAP patients through qPCR, western blot, and immunohistochemistry (IHC) analysis.<h4>Methods</h4>Seventeen patients with FAP admitted to Tianjin Union Medical Center ...[more]

PMID: 33108070

Similar Datasets

Project description:Vascular cyclooxygenase (COX)-2-dependent prostacyclin (PGI(2)) may affect angiogenesis by preventing endothelial activation and platelet release of angiogenic factors present in platelet ?-granules. Thus, a profound inhibition of COX-2-dependent PGI(2) might be associated with changes in circulating markers of angiogenesis. We aimed to address this issue by performing a clinical study with celecoxib in familial adenomatous polyposis (FAP). In nine patients with FAP and healthy controls, pair-matched for gender and age, we compared systemic biosynthesis of PGI(2), thromboxane (TX) A(2), and prostaglandin (PG) E(2), assessing their urinary enzymatic metabolites, 2,3-dinor-6-keto PGF(1?) (PGI-M), 11-dehydro-TXB(2) (TX-M), and 11-?-hydroxy-9,15-dioxo-2,3,4,5-tetranor-prostane-1,20-dioic acid (PGE-M), respectively. The impact of celecoxib (400 mg b.i.d. for 7 days) on prostanoid biosynthesis and 14 circulating biomarkers of angiogenesis was evaluated in FAP. Intestinal tumorigenesis was associated with enhanced urinary TX-M levels, but unaffected by celecoxib, suggesting the involvement of a COX-1-dependent pathway, presumably from platelets. This was supported by the finding that in cocultures of a human colon adenocarcinoma cell line (HT-29) and platelets enhanced TXA(2) generation was almost completely inhibited by pretreatment of platelets with aspirin, a preferential inhibitor of COX-1. In FAP, celecoxib profoundly suppressed PGE(2) and PGI(2) biosynthesis that was associated with a significant increase in circulating levels of most proangiogenesis proteins but also the antiangiogenic tissue inhibitor of metalloproteinase 2. Urinary PGI-M, but not PGE-M, was negatively correlated with circulating levels of fibroblast growth factor 2 and angiogenin. In conclusion, inhibition of tumor COX-2-dependent PGE(2) by celecoxib may reduce tumor progression. However, the coincident depression of vascular PGI(2), in a context of enhanced TXA(2) biosynthesis, may modulate the attendant angiogenesis, contributing to variability in the chemopreventive efficacy of COX-2 inhibitors such as celecoxib.

Dataset Information

Analysis of expression levels of markers associated with tumor proliferation and angiogenesis in familial adenomatous polyposis.

Background

Methods

Results

Conclusion

Publications

Analysis of expression levels of markers associated with tumor proliferation and angiogenesis in familial adenomatous polyposis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets