LncRNA SNHG5 regulates imatinib resistance in chronic myeloid leukemia via acting as a CeRNA against MiR-205-5p

Imatinib resistance has become a major obstacle for the treatment of chronic myeloid leukemia (CML). The present study aimed to investigate the effects of the long non-coding RNA, SNHG5 on imatinib resistance in CML and explored the underlying mechanisms. The quantitative real-time PCR results showed that SNHG5 and ABCC2 expressions were up-regulated in the isolated peripheral blood cells of the CML patients when compared with healthy controls, and SNHG5 expression levels was positively correlated with ABCC2 in CML patients. In vitro studies showed that the expressions of SNHG5 and ABCC2 were up-regulated in imatinib resistant cells (K562-R) when compared to K562 cells. Bioinformatics analysis showed the interaction between SNHG5 and miR-205-5p, which was further confirmed by luciferase reporter assay and RNA immune-precipitation in K562 cells. Overexpression of SNHG5 suppressed the expression of miR-205-5p and the expression of SNHG5 was negatively correlated with the miR-205-5p expression in CML patients. In addition, ABCC2 was predicted as a downstream target of miR-205-5p, which was further confirmed by the luciferase reporter assay in K562-R cells, and overexpression of miR-205-5p suppressed the expression of ABCC2 in K562-R cells. In vitro functional assay showed that overexpression of SNHG5 in K562 cells increased imatinib resistance and knock-down of SNHG5 reduced the imatinib resistance in K562-R cells. Further experiments showed that SNHG5 promotes imatinib resistance through regulating ABCC2. Taken together, SNHG5 promotes imatinib resistance in CML via acting as a competing endogenous RNA against miR-205-5p.