BackgroundMacrophage migration inhibitory factor (MIF) is a widely expressed cytokine involved in a variety of cellular processes including cell cycle regulation and the control of proliferation. Overexpression of MIF has been reported in a number of cancer types and it has previously been shown that MIF is upregulated in melanocytic tumours with the highest expression levels occurring in malignant melanoma. However, the clinical significance of high MIF expression in melanoma has not been reported.MethodsMIF expression was depleted in human melanoma cell lines using siRNA-mediated gene knockdown and effects monitored using in vitro assays of proliferation, cell cycle, apoptosis, clonogenicity and Akt signalling. In silico analyses of expression microarray data were used to correlate MIF expression levels in melanoma tumours with overall patient survival using a univariate Cox regression model.ResultsKnockdown of MIF significantly decreased proliferation, increased apoptosis and decreased anchorage-independent growth. Effects were associated with reduced numbers of cells entering S phase concomitant with decreased cyclin D1 and CDK4 expression, increased p27 expression and decreased Akt phosphorylation. Analysis of clinical outcome data showed that MIF expression levels in primary melanoma were not associated with outcome (HR = 1.091, p = 0.892) whereas higher levels of MIF in metastatic lesions were significantly associated with faster disease progression (HR = 2.946, p = 0.003 and HR = 4.600, p = 0.004, respectively in two independent studies).ConclusionsOur in vitro analyses show that MIF functions upstream of the PI3K/Akt pathway in human melanoma cell lines. Moreover, depletion of MIF inhibited melanoma proliferation, viability and clonogenic capacity. Clinically, high MIF levels in metastatic melanoma were found to be associated with faster disease recurrence. These findings support the clinical significance of MIF signalling in melanoma and provide a strong rationale for both targeting and monitoring MIF expression in clinical melanoma.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2407-14-630) contains supplementary material, which is available to authorized users.

Structural defects are ubiquitous for polycrystalline perovskite films, compromising device performance and stability. Herein, a universal method is developed to overcome this issue by incorporating halide perovskite quantum dots (QDs) into perovskite polycrystalline films. CsPbBr3 QDs are deposited on four types of halide perovskite films (CsPbBr3, CsPbIBr2, CsPbBrI2, and MAPbI3) and the interactions are triggered by annealing. The ions in the CsPbBr3 QDs are released into the thin films to passivate defects, and concurrently the hydrophobic ligands of QDs self‐assemble on the film surfaces and grain boundaries to reduce the defect density and enhance the film stability. For all QD‐treated films, PL emission intensity and carrier lifetime are significantly improved, and surface morphology and composition uniformity are also optimized. Furthermore, after the QD treatment, light‐induced phase segregation and degradation in mixed‐halide perovskite films are suppressed, and the efficiency of mixed‐halide CsPbIBr2 solar cells is remarkably improved to over 11% from 8.7%. Overall, this work provides a general approach to achieving high‐quality halide perovskite films with suppressed phase segregation, reduced defects, and enhanced stability for optoelectronic applications.

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The surface chemistry of colloidal quantum dots (CQD) play a crucial role in fabricating highly efficient and stable solar cells. However, as‐synthesized PbS CQDs are significantly off‐stoichiometric and contain inhomogeneously distributed S and Pb atoms at the surface, which results in undercharged Pb atoms, dangling bonds of S atoms and uncapped sites, thus causing surface trap states. Moreover, conventional ligand exchange processes cannot efficiently eliminate these undesired atom configurations and defect sites. Here, potassium triiodide (KI3) additives are combined with conventional PbX2 matrix ligands to simultaneously eliminate the undercharged Pb species and dangling S sites via reacting with molecular I2 generated from the reversible reaction KI3 ⇌ I2 + KI. Meanwhile, high surface coverage shells on PbS CQDs are built via PbX2 and KI ligands. The implementation of KI3 additives remarkably suppresses the surface trap states and enhances the device stability due to the surface chemistry optimization. The resultant solar cells achieve the best power convention efficiency of 12.1% and retain 94% of its initial efficiency under 20 h continuous operation in air, while the control devices with KI additive deliver an efficiency of 11.0% and retains 87% of their initial efficiency under the same conditions.