Research Paper Volume 12, Issue 17 pp 17459—17479

Figure 2. LINC00160 participates in sunitinib resistance of RCC. (A) LINC00160 expression was compared between resistant and parental cells by RT-qPCR. (B) GSEA analysis revealed that high LINC00160 expression was involved in JAK-STAT signaling pathway. (C) LINC00160 expression was detected by RT–qPCR after knockdown and overexpression. (D) Cell viability assays in sunitinib concentration gradients were conducted after LINC00160 knockdown and overexpression. (E) Transwell assays were conducted after sunitinib treatment and LINC00160 overexpression. (F) Western blotting analysis of p-STAT3 and STAT3 after silencing LINC00160 in resistant cells, upregulating LINC00160 in parental cells and overexpressing LINC00160 combined with sunitinib treatment in parental cells. β-actin served as the loading control. Each experiment was performed at least three times and data was represented as mean ± SEM. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. LINC00160, long non-coding RNA 160; RCC, renal cell carcinoma; RT-qPCR, quantitative real time polymerase chain reaction; GSEA, gene set enrichment analysis; JAK, Janus kinase; p-STAT3, phosphorylated signal transducer and activator of transcription 3; STAT3, signal transducer and activator of transcription 3.