Long Non-coding RNA CASC15 Promotes Intrahepatic Cholangiocarcinoma Possibly through Inducing PRDX2/PI3K/AKT Axis.

摘要: Purpose Intrahepatic cholangiocarcinoma (ICC) is one of the most common liver primary tumors but its treatments are limited. Bioinformatics showed that expression level long non-coding RNA cancer-associated susceptibility 15 gene (CASC15) correlated with ICC progression, functional mechanism remains unclear. Material and methods Tissues from patients, tumor adjacent tissue, were used for detection CASC15. Clinical data also collected clinicopathologic survival analysis. Short interfering lentiviral short hairpin to knock down CASC15 PRDX2 in cell lines, analysis changes function xenografts. RNA-pulldown immunoprecipitation assays detect RNA-binding protein, PRDX2. Male nude mice xenografts, livers after 4 weeks immunohistochemistry. Results highly expressed tissues related higher TNM stage. Knockdown cells reduced proliferation, migration, invasiveness increased apoptosis, G1/S block. bound decreased which was rescued by inhibition proteasome formation. Downregulation resulted block, invasion. inhibited phosphoinositide 3-kinase (PI3K)/AKT/c-Myc pathway through downregulating overexpressed knockout xenografts suppressed development vivo, Ki67 PI3K/AKT pathway. Conclusion promotes possibly targeting via pathway, indicating poor prognosis high degree malignancy ICC.