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Background: Observational studies have showed an association between schizophrenia and risk of psoriasis and vice versa. However, whether schizophrenia is causally associated with psoriasis is unclear. Method s : A two‐sample bidirectional Mendelian randomization (MR) analysis was performed with publicly available genome‐wide association study data including schizophrenia (n = 77 096) and psoriasis (n = 462 933). The inverse‐variance weighted method was performed as the main analysis, with a complementary with the other two analyses: MR‐Egger and weighted median method. A series of sensitivity analyses were also conducted to evaluate the robustness of the results. Results: MR analyses indicated that genetically predicted schizophrenia was significantly associated with an increased risk of psoriasis [OR: 1.001, 95% confidence interval (CI): 1.000–1.002, p = 0.012]. However, no causal effect of genetically predicted psoriasis on schizophrenia (OR: 0.221, 95% CI: 0.029–1.682, p = 0.145) was detected. No pleiotropy or heterogeneity was detected in sensitivity analysis (all p > 0.05). Conclusions: Our study provides genetic evidence for the causal association between schizophrenia and psoriasis. [ABSTRACT FROM AUTHOR]

Sanguinarine (SAG) is the most abundant constituent of Macleaya cordata (Willd.) R. Br. (Popaceae). SAG has shown antimammary and colorectal metastatic effects in mice in vivo, suggesting its potential for cancer chemotherapy. To determine the antimetastatic effect and underlying molecular mechanisms of SAG on melanoma. CCK8 assay was used to determine the inhibition of SAG on the proliferation of A375 and A2058 cells. Network pharmacology analysis was applied to construct a compound-target network and select potential therapeutic targets of SAG against melanoma. Molecular docking simulation was conducted for further analysis of the selected targets. In vitro migration/invasion/western blot assay with 1, 1.5, 2 μM SAG and in vivo effect of 2, 4, 8 mg/kg SAG in xenotransplantation model in nude mice. The key targets of SAG treatment for melanoma were mainly enriched in PI3K-AKT pathway, and the binding energy of SAG to PI3K, AKT, and mTOR were −6.33, −6.31, and −6.07 kcal/mol, respectively. SAG treatment inhibited the proliferation, migration, and invasion ability of A375 and A2058 cells (p < 0.05) with IC50 values of 2.378 μM and 2.719 μM, respectively. It also decreased the phosphorylation levels of FAK, PI3K, AKT, mTOR and protein expression levels of MMP2 and ICAM-2. In the nude mouse xenograft model, 2, 4, 8 mg/kg SAG was shown to be effective in inhibiting tumour growth. Our research offered a theoretical foundation for the clinical antitumor properties of SAG, further suggesting its potential application in the clinic. [ABSTRACT FROM AUTHOR]