In the present study, the potential of curcumin to stimulate proliferation, stemness acting signals and migration of 3T3-L1 preadipocytes and the associated molecular mechanisms were investigated. Low concentrations of curcumin stimulated cell proliferation, whereas high concentrations were cytotoxic to 3T3-L1 cells. In particular, application of 0.02 µM of curcumin for 24 h resulted in significantly increased cell proliferation and was determined to be the optimal treatment for this study. In a colony-forming cell assay, cells treated with 0.02 µM of curcumin showed an approximately 1.5-fold increase in colony formation. Curcumin treatment up-regulated the proliferation-related marker proteins coupled with increased cell growth, telomerase activity and overexpression of stemness acting signals, which was associated with activation of the phosphoinositide 3-kinase (PI3K) pathway. In addition, curcumin significantly inactivated p38 mitogen-activated protein kinases (MAPK) and stress-activated protein kinase/c-Jun N-terminal kinases (SARK/JNK), coupled with inhibition of p53 and p21 tumor suppressor gene products. In addition, curcumin significantly increased cell migration through activation of migration-associated transcription factors. Therefore, these results clearly show that activation of cell proliferation by curcumin is associated with improved stem cell potency in 3T3-L1 preadipocytes.

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