Fig. 6. HOTTIP may promote SCLC chemoresistance and pathogenesis through ceRNA mechanism.

a Putative binding site of miR-216a in HOTTIP and BCL-2 3’-UTR and the site of target mutagenesis are indicated. b miR-216a may negatively regulated expression of its target genes HOTTIP and BCL-2. c miR-216a may negatively regulated expression of HOXA13 and BCL-2 proteins. d HOTTIP may positively regulated expression of BCL-2 in H69AR cell. e The relevance analysis of HOTTIP and BCL-2 expression in SCLC FFPE tissues. f–h Luciferase activity of the indicated group in H69AR cell. i, j RNA pull-down, mass spectrometry and western blot showed a possible interaction exists between HOTTIP and Ago2. k RIP assay of the enrichment of Ago2 on HOTTIP and BCL-2 transcripts relative to IgG in H69AR cell transfected with si-HOTTIP. *P < 0.05; **P < 0.01; ***P < 0.001