RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/38293991http://www.w3.org/2000/01/rdf-schema#comment"

Objective

To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil (5-FU) resistance in cholangiocarcinoma cells.

Methods

HCCC-9810 cells were used to construct a 5-FU-resistant cell model (HCCC-9810/5-FU cells), and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1, Beclin1, LC3 and P62 were detected with qRT-PCR and Western blotting. The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay, and the changes in expressions of SOX2OT, SIRT1, Beclin1, LC3 and P62 were detected. Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance. A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.

Results

The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU (P < 0.05). The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1, Beclin1 and p62, an increased LC3 Ⅱ/LC3 Ⅰ ratio, and enhanced expressions of SIRT1 mRNA and SOX2OT (P < 0.05). Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1, Beclin1 and p62, the LC3Ⅱ/LC3Ⅰ ratio, and expression levels of SIRT1 mRNA and SOX2OT (P < 0.05), and these changes were obviously attenuated by SIRT1 knockdown, which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT (P > 0.05). RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.

Conclusion

LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.org/dc/terms/identifier"doi:10.12122/j.issn.1673-4254.2024.01.22"xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Li X."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Yang S."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Wang X.'"xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Ning J."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/author"Xin C."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/date"2024"xsd:gYear
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/name"Nan Fang Yi Ke Da Xue Xue Bao"xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/pages"187-193"xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/title"[LncRNA SOX2OT enhances 5-fluorouracil resistance of cholangiocarcinoma cells by promoting autophagy via up-regulating SIRT1 expression]."xsd:string
http://purl.uniprot.org/citations/38293991http://purl.uniprot.org/core/volume"44"xsd:string
http://purl.uniprot.org/citations/38293991http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/38293991
http://purl.uniprot.org/citations/38293991http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/38293991
http://purl.uniprot.org/uniprot/#_E9PC49-mappedCitation-38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38293991
http://purl.uniprot.org/uniprot/#_A8K128-mappedCitation-38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38293991
http://purl.uniprot.org/uniprot/#_A0A9Y1ZCD8-mappedCitation-38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38293991
http://purl.uniprot.org/uniprot/#_B0QZ35-mappedCitation-38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38293991
http://purl.uniprot.org/uniprot/#_B3KNK3-mappedCitation-38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38293991
http://purl.uniprot.org/uniprot/#_I1Y8W7-mappedCitation-38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38293991
http://purl.uniprot.org/uniprot/#_Q96EB6-mappedCitation-38293991http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38293991