Involvement of CHOP in activin A‑induced myeloma NS‑1 cell apoptosis

Activin A, a multifunctional cytokine, is a member of transforming growth factor‑β (TGF‑β) superfamily. It is associated with a variety of pathophysiological processes, including inflammation, fibrosis, and tumorigenesis. Chronic or prolonged endoplasmic reticulum (ER) stress can lead to cells apoptosis. However, whether ER stress‑related proteins, such as CHOP, GADD34 are involved in activin A‑induced myeloma cell apoptosis remains unknown. In the present study, it was revealed that activin A inhibited the proliferation of myeloma cell line NS‑1 cells and induced NS‑1 cell apoptosis. Activin A upregulated the expression of CHOP, GADD34, caspase‑3, and caspase‑12. Moreover, both Smad3 and p‑Smad3 levels were increased with treatment of activin A. Further studies revealed that the overexpression of activin signaling protein Smad3 in NS‑1 cells increased the levels of CHOP, caspase‑3, and p‑Smad3. These data indicated that the CHOP protein of the ER stress pathway may be involved in activin A‑induced NS‑1 cell apoptosis, and also indicated the potential therapy of activin A‑induced apoptosis via CHOP signaling for multiple myeloma.