Long non-coding RNA Sox2 overlapping transcript (SOX2OT) was reported to be involved in progression of multiple cancers. However, the role and mechanism of SOX2OT in multiple myeloma (MM) has yet to be unravelled. In the present study, elevated SOX2OT levels are reported in MM cell lines and patient samples as compared to normal plasma cells (nPCs) and healthy donors, respectively. Knock-down of SOX2OT led to a significant inhibition of cell proliferation, arrested cells at G0/G1 phase and induced cell apoptosis in MM samples in vitro, as well as slowed the growth of tumours in vivo. Additionally, our data indicated that SOX2OT functioned as a competing endogenous RNA (ceRNA) in MM cells that regulated miR-144-3p expression. Repression of miR-144-3p reversed the inhibition of MM development due to SOX2OT knock-down. Our data also revealed that SOX2OT regulated the expression of the cellular-mesenchymal to epithelial transition factor (c-MET, a known target of miR-143-3p) by functioning as a sponge of miR-144-3p in MM samples. These data support that SOX2OT promotes MM progression through regulating the miR-144-3p/c-MET axis, suggesting that SOX2OT might be as a potential therapeutic target for MM. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.Vitiligo is the most common acquired pigmentary disorder, which afflicts 0.5-1% of the world population, and is characterized by depigmented skin patches resulting from melanocyte loss. Vitiligo has a complex etiology, and varies in its manifestations, progression, and response to treatment. It presents as an autoimmune disease, evidenced by circulating melanocyte-specific antibodies, and association with other autoimmune diseases. However, autoimmunity may be secondary to the high oxidative stress in vitiligo skin and to intrinsic defects in melanocytes and their microenvironment, which contribute to aberrant stress response, neo-antigenicity, and susceptibility of melanocytes to immune attack and apoptosis. There is also a genetic predisposition to vitiligo, which sensitizes melanocytes to environmental agents, such as phenolic compounds. Currently, there are different treatment modalities for re-pigmenting vitiligo skin. However, when repigmentation is achieved, the major challenge is maintaining the pigmentation, which is lost in 40% of cases. In this review, we present an overview of the clinical aspects of vitiligo, its pathophysiology, the intrinsic defects in melanocytes and their microenvironment, and treatment strategies. Based on lessons from the biology of human melanocytes, we present our perspective of how repigmentation of vitiligo skin can be achieved and sustained. This article is protected by copyright. All rights reserved.Bone defects resulting from non-union fractures or tumour resections are common clinical problems. Long non-coding RNAs (lncRNAs) are reported to play vital roles in stem cell differentiation. The aim of this study was to elucidate the role of lncRNA-H19 in osteogenic differentiation of bone marrow mesenchymal stem cells (BMMSCs). Following the establishment of an osteogenic differentiation model in rats, the expression of H19, microRNA-149 (miR-149) and stromal cell-derived factor-1 (SDF-1) was measured by RT-qPCR. Thereafter, BMMSCs were isolated from rats and treated with a series of mimic, inhibitor or siRNA. SDF-1 expression, alkaline phosphatase (ALP) activity and osteocalcin (OCN) content were detected. The mineralized and calcified nodules were assessed by alizarin red S and Von Kossa staining. BMMSC surface markers were detected by flow cytometry. Western blot analysis was used to measure the expression of ALP, OCN, runt-related transcription factor 2 (RUNX2) and osterix (OSX) proteins. Lastly, dual-luciferase reporter gene assay and RNA immunoprecipitation were applied to verify the relationship of H19, miR-149 and SDF-1. Overexpressed H19 and SDF-1 and poorly expressed miR-149 were found in rats with osteogenic differentiation. H19 increased SDF-1 expression by binding to miR-149. H19 enhanced ALP activity, OCN content, calcium deposit and ALP, OCN, RUNX2 and OSX protein expression of BMMSCS by up-regulating SDF-1 via binding to miR-149. Taken together, up-regulated H19 could promote the osteogenic differentiation of BMMSCs by increasing SDF-1 via miR-149. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.Marfan Syndrome (MFS) is an autosomal dominant connective tissue disorder with a wide range of severities. Ninety-five percent of MFS probands have a mutation in the fibrillin-1 gene (FBN1); however, there are a high number of unique mutations complicating attempts at establishing any phenotype-genotype correlations for this disease (Tiecke et al., European Journal of Human Genetics, 2001, 9, 13-21). One of the few extant genotype-phenotype correlations is in exon 24-32 which have been associated with a severe pediatric presentation of neonatal MFS with predominately cardiovascular symptoms. We present a 24-year-old male patient with a heterozygous de novo variant NM_000138.4 c.3037G>A (p.G1013R) located in exon 25 of the FBN1 gene. The patient was found to have dysplastic mitral and tricuspid valves with dilated aortic root at 9 months of age. This is a notable case in that the location of this patient’s mutation and his age of symptom onset would indicate a guarded prognosis. Further, this mutation, FBN1 G1013R, has been reported in the literature in four other unrelated patients all of whom presented at a young age with cardiac involvement and all of whom had relative longevity when compared to other patients with mutations in this exon 24-32 hot spot. Shield-1 These findings may represent a more specific genotype-phenotype correlation within this mutational hot spot. © 2020 Wiley Periodicals, Inc.The NK cell compartment provides powerful innate defenses against virus-infected and tumor cells. Specific NK cell receptors control this process and maintain the immune system homeostasis and prevent autoimmunity. A wide variety of NK cell subsets with different functional capabilities exist and this reflects not only the different maturation stages of NK cells but also different microenvironments in which they can operate. In this review, we will give an overview on the various NK cell subsets present in peripheral blood of healthy donors in order to clearly and univocally identify them on the basis of their phenotypic traits using flow cytometry. © 2020 International Society for Advancement of Cytometry.