[No authors listed]
Recent evidence indicates that the long nonâcoding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is involved in tumorigenesis of several types of cancer through targeting microRNAs (miRs); however, the molecular mechanism of CASC2 in pancreatic cancer remains elusive. In the present study, the expression levels of CASC2, miRâ24 and mucin 6 (MUC6) were measured in pancreatic cancer specimens and cell lines by reverse transcriptionâquantitative PCR. Western blotting was used to determine the protein expression levels of MUC6, Integrin β4 (ITGB4), phosphorylated (p)âfocal adhesion kinase (FAK) and several epithelialâtoâmesenchymal transition markers in pancreatic cancer cells. MTT, colony formation, wound healing, Transwell and flow cytometry assays were performed to detect cell proliferation, colony formation, migration, invasion and apoptosis, respectively, in vitro. Morphological changes of pancreatic cancer cells were assessed by light microscopy. The interactions between CASC2, miRâ24 and MUC6 were assessed by the dualâluciferase reporter assay. A tumor xenograft model was generated to investigate tumor growth in vivo. CASC2 and MUC6 were downregulated, and miRâ24 was upregulated in pancreatic cancer specimens and cell lines. Functionally, CASC2 overexpression or miRâ24 knockdown suppressed pancreatic cancer cell proliferation, colony formation, migration and invasion, and promoted apoptosis. Additionally, they altered cellâcell adhesion as demonstrated by the attenuated ITGB4, pâFAK and Nâcadherin protein levels, as well as morphological changes. Mechanistically, CASC2 sponged miRâ24 and activated its downstream target MUC6 to suppress pancreatic cancer growth and progression. CASC2 exerted tumorâsuppressive functions in pancreatic cancer through the miRâ24/MUC6 axis, which may be a promising target for pancreatic cancer therapy.
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