Fig. 3From: LncRNA HOTAIR induces sunitinib resistance in renal cancer by acting as a competing endogenous RNA to regulate autophagy of renal cellsEffect of cell autophagy on sunitinib resistance in RC cells. To verify the regulatory role of cell autophagy in sunitinib resistance of RC cells, the parental cells (786-O and ACHN) were subjected to RAP for activation of cell autophagy. Meanwhile, sunitinib-resistant cells (786-O-R and ACHN-R) were exposed to 3-MA for inhibition of cell autophagy. Increased autophagic vacuoles of parental cells after RAP treatment as well as reduced autophagic vacuoles of sunitinib-resistant cells after 3-MA subjection were conducted by MDC staining (a). The enhanced fluorescence intensity of LC3 in RAP-induced group and suppressed fluorescence intensity of LC3 in the 3-MA-treated group were estimated by immunofluorescence (b). Protein expressions of LC3-II/LC3-I and p62 were assessed by Western blot. RAP potentiated LC3-II/LC3-I protein levels and lowered p62 expression in 786-O and ACHN cells. In 786-O-R and ACHN-R cells, 3-MA elevated protein expression of p62 and restrained LC3-II/LC3-I levels (c). CCK-8 assay was utilized to test the RC cell sensitivity to sunitinib. RAP was found to enhance the sunitinib resistance of parental cells, while 3-MA was discovered to potentiate the sunitinib sensitivity of sunitinib-resistant cells (d). Colony formation was applied to observe the formation of clone after exposure to 10 μM of sunitinib or DMSO. RAP-treated group had increased colony formation, while 3-MA-treated group possessed lowered colony formation (e). *P < 0.05, **P < 0.01, compared to 786-O + Control group or 786-O-R + Control group; #P < 0.05, ##P < 0.01, compared to ACHN + Control or ACHN-R + Control group; RC, renal cancer; RAP, rapamycin; 3-MA, 3-methyladenineBack to article page