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Fig. 2 | Cancer Cell International

Fig. 2

From: LncRNA HOTAIR induces sunitinib resistance in renal cancer by acting as a competing endogenous RNA to regulate autophagy of renal cells

Fig. 2

Effect of HOTAIR knockdown on autophagy and sunitinib resistance in 780-O-R and ACHN-R cells. Highly expressed HOTAIR and Beclin1 as well as lowly expressed miR-17-5p in RC tissues were inspected by qRT-PCR in comparison to those in para-carcinoma tissues (a). The negative correlation of miR-17-5p and HOTAIR or Beclin1, as well as positive correlation between HOTAIR and Beclin1 were detected (b). The parental and sunitinib-resistant cells were transfected with sh-HOTAIR. qRT-PCR accessed that transfection with sh-HOTAIR restrained the mRNA level of HOTAIR in RC cell lines (c). Then the effect of HOTAIR knockdown on cell autophagy was performed. Reduced autophagic vacuoles detected by MDC staining were found in RC cells which transfected with sh-HOTAIR (d). Immunofluorescence performed that expression intensity of LC3 was diminished after sh-HOTAIR transfection (e). The elevated protein expression of p62 and reduced LC3-II/LC3-I ratio in RC cells transfected with sh-HOTAIR were evaluated by Western blot (f). After cell transfection of sh-HOTAIR, sensitivity of RC cells to sunitinib was determined. The enhanced sensitivity of RC cells to sunitinib was measured by CCK-8 assay (g). After RC cells treated with 10 μM sunitinib or DMSO, the inhibited cell colony formation ability was assessed using colony formation assay (h). *P < 0.05, **P < 0.01, compared to 786-O or ACHN group; #P < 0.05, ##P < 0.01, compared to 786-O-R or ACHN-R group; RC, renal cancer; DMSO, dimethylsulfoxide

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