Fig. 4.

Overexpression of NUPR1 partially reversed the role of miR‐637 in inhibiting proliferation, autophagy, and promoting apoptosis. (A, B) The cell viability of MM cells after transfecting miR‐637 mimics, NC‐LV, or NUPR1‐LV was determined by CCK‐8 assay. Comparison was performed between the NUPR1‐LV + miR‐637 mimic group and the miR‐637 mimic group. The viability rate of U266 cells was higher in the NUPR1‐LV + miR‐637 mimic group than that in the miR‐637 mimic group at 1d, 2d, 3d, 4d, and 5d (P = 0.042, 0.005, and 0.003, respectively). Likewise, the viability rate of RPMI8266 in the NUPR1‐LV + miR‐637 mimic group was significantly increased, as compared with miR‐637 mimics at 1d, 2d, 3d, 4d, and 5d (P = 0.049, 0.006, and 0.007, respectively). (C, D) The apoptosis of MM cells was detected by flow cytometry (n = 3, Student’s t‐test). (E) The protein expression of Bax, Bcl2, cleaved caspase 3, P62, and LC3 was detected by western blot. β‐actin was served as loading control. Data are shown as mean ± SD of three independent experiments (n = 3, one‐way ANOVA). *P < 0.05, **P < 0.01, and ***P < 0.001.