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http://purl.uniprot.org/citations/31308265http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31308265http://www.w3.org/2000/01/rdf-schema#comment"Aberrant expressions of various long non-coding RNAs (lncRNAs) have been involved in the progression and pathogenesis of various carcinomas. However, the expression and biological function of SLCO4A1-AS1 in colorectal cancer (CRC) remain poorly understood. Gain- and loss-of-function assays were applied to determine the roles of SLCO4A1-AS1 in autophagy and CRC progression. qRT-PCR and in situ hybridization (ISH) results showed that SLCO4A1-AS1 was positively associated with PARD3 expression in CRC tissues. In vitro and in vivo studies revealed that SLCO4A1-AS1 knockdown repressed cytoprotective autophagy as assayed by transmission electron microscopy (TEM), and inhibited cell proliferation by directly targeting partition-defective 3 (PARD3). Mechanistically, SLCO4A1-AS1 acted as a sponge of miR-508-3p, leading to upregulation of PARD3 and promotion of CRC cell proliferation. The current study demonstrates that the SLCO4A1-AS1/miR-508-3p/PARD3/autophagy pathway play a critical role in CRC cell proliferation, and might provide novel targets for developing therapeutic strategies for CRC."xsd:string
http://purl.uniprot.org/citations/31308265http://purl.org/dc/terms/identifier"doi:10.18632/aging.102081"xsd:string
http://purl.uniprot.org/citations/31308265http://purl.uniprot.org/core/author"Jin J."xsd:string
http://purl.uniprot.org/citations/31308265http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/31308265http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31308265http://purl.uniprot.org/core/name"Aging (Albany NY)"xsd:string
http://purl.uniprot.org/citations/31308265http://purl.uniprot.org/core/pages"4876-4889"xsd:string
http://purl.uniprot.org/citations/31308265http://purl.uniprot.org/core/title"LncRNA SLCO4A1-AS1 promotes colorectal cancer cell proliferation by enhancing autophagy via miR-508-3p/PARD3 axis."xsd:string
http://purl.uniprot.org/citations/31308265http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/31308265http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31308265
http://purl.uniprot.org/citations/31308265http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31308265
http://purl.uniprot.org/uniprot/#_Q8TEW0-mappedCitation-31308265http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/#_Q8TB00-mappedCitation-31308265http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/#_Q8IX26-mappedCitation-31308265http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/#_Q8IX27-mappedCitation-31308265http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/#_Q8IX28-mappedCitation-31308265http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/Q8IX27http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/Q8TEW0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/Q8IX28http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/Q8IX26http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31308265
http://purl.uniprot.org/uniprot/Q8TB00http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31308265