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

class="figure-viewer-img"

Figure 4. SAA1 mediates sunitinib resistance of RCC. (A) SAA1 expression was detected by RT–qPCR and western blotting after knockdown and overexpression. (B) Cell viability assays in sunitinib concentration gradients were conducted after SAA1 knockdown and overexpression. (C) Transwell assays were conducted after sunitinib treatment and SAA1 overexpression. (D) Western blotting analysis of p-STAT3 and STAT3 after silencing SAA1 in resistant cells, upregulating SAA1 in parental cells and overexpressing SAA1 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. SAA1, serum amyloid A1; RCC, renal cell carcinoma; RT-qPCR, quantitative real time polymerase chain reaction; p-STAT3, phosphorylated signal transducer and activator of transcription 3; STAT3, signal transducer and activator of transcription 3.