Resveratrol (Res), a natural plant extract, is an effective inducer of cell apoptosis and cell cycle arrest in multiple carcinoma cell types, which has been demonstrated by its ability to inhibit the proliferation of multiple human tumor cells in vitro. Although Res possesses chemopreventive properties against several types of cancer, the molecular mechanism underlying its anticancer activity remains to be fully elucidated. The present study demonstrated that Res induced cell cycle arrest and inhibited the proliferation of human melanoma A375 (IC50=23 µM after 48 h; P<0.05) and SK-MEL-31 (IC50=15 µM after 48 h; P<0.05) cells. Western blot analysis demonstrated that Res induced the apoptosis of human melanoma A375 and SK-MEL-31 cells by upregulating the expression of Bcl-2-associated X protein and B-cell lymphoma 2, possibly via the p53 pathway and activation of caspase-9 and caspase-3.
Background
Dual specificity phosphatase 22 (DUSP22) plays an important role in the regulation of immune and inflammation, but its correlation with clinical features and treatment outcome in psoriasis patients is still unclear. This study was to investigate the longitudinal change of DUSP22 with time, as well as its association with disease activity and treatment response in psoriasis patients.
Methods
Totally, 120 psoriasis patients, 50 patients with other skin inflammations as disease controls (DCs), and 50 health controls (HCs) were recruited. Serum samples were collected from psoriasis patients at baseline, month (M)1, M3, and M6 after initiation of etanercept‐based treatment as well as from DCs and HCs after enrollment to assess DUSP22 level by enzyme‐linked immunosorbent assay.
Results
DUSP22 was lower in psoriasis patients than in HCs and DCs (both p < 0.001). Besides, in psoriasis patients, DUSP22 was associated with lower psoriasis area severity index (PASI) score (p = 0.001) and systemic biological treatment history (p = 0.023), but not with other demographics, disease characteristics, or treatment history (all p>0.05). In addition, DUSP22 was increased with time (p < 0.001) in total patients. Moreover, DUSP22 at M3 (p = 0.004) and M6 (p < 0.001) was higher in response patients than in non‐response patients evaluated by PASI 75. Additionally, DUSP22 at M3 (p < 0.001) and M6 (p = 0.003) was also increased in response patients compared with non‐response patients evaluated by PASI 90.
Conclusion
DUSP22 decreases and negatively correlates with disease activity, while its longitudinal elevation with time reflects satisfactory treatment response in psoriasis patients.
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