RESUMEN
Activin A, a multifunctional cytokine, is a member of transforming growth factorß (TGFß) 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 stressrelated proteins, such as CHOP, GADD34 are involved in activin Ainduced myeloma cell apoptosis remains unknown. In the present study, it was revealed that activin A inhibited the proliferation of myeloma cell line NS1 cells and induced NS1 cell apoptosis. Activin A upregulated the expression of CHOP, GADD34, caspase3, and caspase12. Moreover, both Smad3 and pSmad3 levels were increased with treatment of activin A. Further studies revealed that the overexpression of activin signaling protein Smad3 in NS1 cells increased the levels of CHOP, caspase3, and pSmad3. These data indicated that the CHOP protein of the ER stress pathway may be involved in activin Ainduced NS1 cell apoptosis, and also indicated the potential therapy of activin Ainduced apoptosis via CHOP signaling for multiple myeloma.