Research Paper Volume 12, Issue 17 pp 17459—17479

LINC00160 mediates sunitinib resistance in renal cell carcinoma via SAA1 that is implicated in STAT3 activation and compound transportation

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Figure 3. SAA1 is a candidate downstream molecule of LINC00160 in RCC cells. (A) Heatmap analysis of TCGA-KIRC samples (N=535) ranking LINC00160 expression from high to low. (B) Candidate mRNAs selected from GSEA analysis and correlation analysis. (C) Candidate genes expressions were verified in resistant and parental cells by RT-qPCR. (D) Correlation between SAA1 and LINC00160 expression. (E) Western blotting analysis of SAA1 after silencing LINC00160 in resistant cells, upregulating LINC00160 in parental cells and comparison between parental and resistant cells. β-actin served as the loading control. (F) GO analysis of SAA1 in enrichment pathways. Enrichment pathways of SAA1 after GO analysis. Each experiment was performed at least three times and data was represented as mean ± SEM. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 and P>0.05 is denoted by ns. SAA1, serum amyloid A1; LINC00160, long non-coding RNA 160; RCC, renal cell carcinoma; TCGA-KIRC, the cancer genome atlas program- kidney renal clear cell carcinoma; GSEA, gene set enrichment analysis; RT-qPCR, quantitative real time polymerase chain reaction; GO, gene ontology.