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. 2014 Apr 15;8(7):1208–1219. doi: 10.1016/j.molonc.2014.03.019

Figure 3.

Figure 3

Dysregulation of miR‐944 contributes to tumorigensis of NSCLC by targeting SOCS4. A, forced expression of miR‐944 in CALU‐1 cells increased cell growth. B, ectopic expression of miR‐944 in CALU‐1 cells augmented cell proliferation. C, ectopic expression of miR‐944 in CALU‐1 promoted cell invasion and migration. The experiments were performed in two cell lines, CALU‐1 and H520, and produced similar data. Figures A–C only showed the results from CALU‐1 cells. D, a miR‐944 target site within 3′‐UTR of SOCS4 was predicted by bioinformatic algorithms. E, a luciferase reporter assay in CALU‐1 cells showed that luciferase activity of SOCS4‐3’UTR was inhibited by increased miR‐944 expression. F, Consequently, protein expression of SOCS4 was reduced. G, SK‐MES‐1 cells that had a high endogenous miR‐944 level after transfection with miR‐944 inhibitor showed a lower miR‐944 level determined by qRT‐PCR (left), but a higher SOCS4 level compared with cells treated with control (right). All data were obtained from three independent experiments and shown as mean ± SD.