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http://purl.uniprot.org/citations/35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35154481http://www.w3.org/2000/01/rdf-schema#comment"Background: The cytoskeletal linker protein α-Catulin has been shown to be important for tumor progression in various cancers. However, its role in the regulation of cancer stemness remains unclear. Methods: Phenotypic effects of α-Catulin on the cancer stem cell (CSC)-like properties and metastasis were examined by in vitro sphere formation assay, migration assay, invasion assay, and in vivo xenografted animal models. Yeast two-hybrid assay, co-immunoprecipitation assay, and cycloheximide chase assay were performed to confirm the effect of α-Catulin on the WWP1-mediated degradation of KLF5. CPTAC and TCGA database were analyzed to determine the clinical association of α-Catulin, KLF5, and stemness-associated signatures in lung adenocarcinoma. Results: We report that α-Catulin increases cancer stem-like properties in non-small cell lung cancer (NSCLC). The expression of α-Catulin is elevated in tumor spheres compared to sphere-derived adherent cells and promotes the acquisition of cancer stemness characteristics in vitro and in vivo. Mechanistically, the interaction of α-Catulin and the C-terminal region of Kruppel-like transcription factor KLF5 results in the inhibition of WWP1-mediated degradation of KLF5. Accordingly, increased protein expression of KLF5 is observed in clinical specimens of lung adenocarcinoma with high expression of α-Catulin compared to specimens with low α-Catulin-expression. Knockdown of KLF5 abrogates α-Catulin-driven cancer stemness. α-Catulin is known to interact with integrin-linked kinase (ILK). Notably, an ILK inhibitor disrupts the α-Catulin-KLF5 interaction, promotes the degradation of KLF5, and decreases α-Catulin-driven cancer stemness. Importantly, we identify a CTNNAL1/ILK/KLF5 three-gene signature for predicting poor overall survival in patients with lung adenocarcinoma. Conclusions: These findings reveal a molecular basis of α-Catulin-enhanced KLF5 signaling and highlight a role for α-Catulin in promoting cancer stemness."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.org/dc/terms/identifier"doi:10.7150/thno.63627"xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Chen Y.L."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Hsu C.L."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Wu Y.Y."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Hong T.M."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Wu J.E."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Huang M.F."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Liang C.H."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/author"Tung C.H."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/name"Theranostics"xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/pages"1173-1186"xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/title"alpha-Catulin promotes cancer stemness by antagonizing WWP1-mediated KLF5 degradation in lung cancer."xsd:string
http://purl.uniprot.org/citations/35154481http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/35154481http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/35154481
http://purl.uniprot.org/citations/35154481http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/35154481
http://purl.uniprot.org/uniprot/#_A0A0A0N0L4-mappedCitation-35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35154481
http://purl.uniprot.org/uniprot/#_A0A0A0N0L7-mappedCitation-35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35154481
http://purl.uniprot.org/uniprot/#_A0A0A0N0M4-mappedCitation-35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35154481
http://purl.uniprot.org/uniprot/#_B3KMX6-mappedCitation-35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35154481
http://purl.uniprot.org/uniprot/#_B2RBI4-mappedCitation-35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35154481
http://purl.uniprot.org/uniprot/#_A8K9T5-mappedCitation-35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35154481
http://purl.uniprot.org/uniprot/#_B4E2I1-mappedCitation-35154481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35154481