Mechanistic studies revealed that Sprouty homolog 2 (SPRY2) was a direct target of miR-27 and that rescuing SPRY2 expression reversed the promoting effects of miR-27 on MM cell proliferation, migration, and invasion.
In summary, we report for the first time that spry2 can inhibit MM cell growth and survival with a concomitant reduction in phosphorylation of extracellular signal-regulated kinases 1 and 2 in vitro and in vivo.
Real-time quantitative PCR and western blot analysis showed that in the MM cell lines with high endogenous miR-21 expression (RPMI8226 and KM3), SPRY2 expression was significantly lower.
The grayscale value of protein bands demonstrated that SPRY2 protein expression significantly decreased in miR‑21 mimic‑transfected U‑266 cells compared with that in the inhibitor‑transfected, siRNA‑transfected and untreated cells (P<0.01). miR‑21 may represent a negative regulator involved in the downregulation of SPRY2 in MM. miR‑21 is closely associated with the pathogenesis, progression and prognosis of MM and may thus be used as an indicator of poor MM prognosis.