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http://purl.uniprot.org/citations/33663522http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/33663522http://www.w3.org/2000/01/rdf-schema#comment"

Background

The epigenetic abnormality of tumor-associated genes contributes to the pathogenesis of colorectal carcinoma (CRC). However, methylation in colorectal cancer is still poorly characterized.

Method

By integration of DNA methylation data from the GEO database and gene expression data from The Cancer Genome Atlas database, the aberrantly methylated genes involved in CRC tumorigenesis were identified. Subsequent in vitro experiments further validated their role in CRC.

Results

We performed integrative genomic analysis and identified HPSE2, a novel tumor suppressor gene that is frequently inactivated through promoter methylation in CRC. K-M survival analysis showed that hypermethylation-low expression of heparanase 2 (HPSE2) was related to poor patient prognosis. Overexpression of HPSE2 reduced cell proliferation in vivo and in vitro. HPSE2 could regulate the p53 signaling pathway to block the cell cycle in G1 phase.

Conclusion

HPSE2, a novel tumor suppressor gene that is frequently inactivated through promoter methylation in CRC. HPSE2 performs a tumor suppressive function by activating the p53/ p21 signaling cascade. The promoter hypermethylation of HPSE2 is a potential therapeutic target in patients with CRC, especially those with late-stage CRC."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.org/dc/terms/identifier"doi:10.1186/s12967-021-02770-0"xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Jiang F."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Wu J."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Shi C."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Xu C."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Feng J."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Ma R."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/author"Qian T."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/name"J Transl Med"xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/pages"98"xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/title"Hypermethylation of heparanase 2 promotes colorectal cancer proliferation and is associated with poor prognosis."xsd:string
http://purl.uniprot.org/citations/33663522http://purl.uniprot.org/core/volume"19"xsd:string
http://purl.uniprot.org/citations/33663522http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/33663522
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