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http://purl.uniprot.org/citations/36472725http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36472725http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Colorectal cancer is one of the most common gastrointestinal tumors. The role of Wnt7b as a ligand of the Wnt signaling pathway in colorectal cancer remains to be studied. Through bioinformatics online analysis, we found that Wnt7b is abnormally highly expressed in a variety of gastrointestinal tumors. This study mainly explored the effects of Wnt7b regulating the Wnt/β-catenin signaling pathway on the proliferation, migration, and invasion of SW480 cells in colorectal cancer.

Methods and results

Applying the TCGA data set, Wnt7b was found to be highly expressed in most gastrointestinal tumor samples. Real-time quantitative PCR(q-PCR), Western blotting(WB) results showed that Wnt7b was significantly higher expressed in colorectal cancer cell lines compared with normal intestinal epithelial cells. SW480 cells transfected with the sh-Wnt7b showed successful knockdown of Wnt7b. MTT colorimetry showed the proliferation ability of sh-Wnt7b group decreased significantly compared with the non-transfected group. The results of double staining flow cytometry showed that the sh-Wnt7b group had more apoptosis. Cell scratch test showed that the cell migration rate of sh-wnt7b group considerably reduced. The Transwell invasion experiment demonstrated that the number of cell invasions in the sh-Wnt7b group decreased significantly. After SW480 cells was transfected with sh-Wnt7b, the protein levels of β-catenin, CCND1, and CD44 in this group of cells were detected to be reduced by WB, and the same results were obtained by q-PCR detection of mRNA.

Conclusion

Wnt7b is highly expressed in colorectal cancer cells, which may affect the proliferation, migration, and invasion of colorectal cancer cells by activating the Wnt/β-catenin signaling pathway."xsd:string
http://purl.uniprot.org/citations/36472725http://purl.org/dc/terms/identifier"doi:10.1007/s11033-022-08106-5"xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/author"Chen S."xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/author"Guo K."xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/author"Wang K."xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/author"Ding H."xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/name"Mol Biol Rep"xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/pages"1415-1424"xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/title"Inhibition of Wnt7b reduces the proliferation, invasion, and migration of colorectal cancer cells."xsd:string
http://purl.uniprot.org/citations/36472725http://purl.uniprot.org/core/volume"50"xsd:string
http://purl.uniprot.org/citations/36472725http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/36472725
http://purl.uniprot.org/citations/36472725http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/36472725
http://purl.uniprot.org/uniprot/#_P56706-mappedCitation-36472725http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36472725
http://purl.uniprot.org/uniprot/#_A8K0G1-mappedCitation-36472725http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/36472725
http://purl.uniprot.org/uniprot/P56706http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36472725
http://purl.uniprot.org/uniprot/A8K0G1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/36472725