The migration and invasion of colon cancer cells were considerably promoted by overexpressed NEAT1. Both NEAT1 and IGF2 bound to miR-185-5p. CONCLUSION NEAT1 upregulate IGF2 expression through absorbing miR-185-5p to enhances the migration and invasion of colon cancer cells. © 2020 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.BACKGROUND Increasing numbers of studies have demonstrated that circulating tumor cells (CTCs) undergo a phenotypic change termed epithelial-mesenchymal transition (EMT), and researchers have proposed that EMT might provide CTCs with increased potential to survive in the different microenvironments encountered during metastasis through various ways, such as by increasing cell survival and early colonization. However, the exact role of EMT in CTCs remains unclear. METHODS In this study, we identified CTCs of 41 patients with gastric cancer using Cyttel-CTC and im-FISH (immune-fluorescence in situ hybridization) methods, and tested the expression of EMT markers and ULBP1 (a major member of the NKG2D-natural killer [NK] group 2 member D-ligand family) on CTCs. Moreover, we investigated the relationship between the expression of EMT markers and ULBP1 on CTCs and gastric cancer cell lines. RESULTS Our results showed that the CTCs of gastric cancer patients exhibited three EMT marker subtypes, and that the expression of ULBP1 was significantly lower on mesenchymal phenotypic CTCs (M+ CTCs) than on epithelial phenotypic CTCs (E+ CTCs). Selleck Tenalisib EMT induced by TGF-β in vitro produced a similar phenomenon, and we therefore proposed that EMT might be involved in the immune evasion of CTCs from NK cells by altering the expression of ULBP1. CONCLUSIONS Our study indicated that EMT might play a vital role in the immune invasion of CTCs by regulating the expression of ULBP1 on CTCs. These findings could provide potential strategies for targeting the immune evasion capacity of CTCs. © 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.Progress of thermal tumor therapies and their translation into clinical practice are limited by insufficient nanoparticle concentration to release therapeutic heating at the tumor site after systemic administration. Herein, the use of Janus magneto-plasmonic nanoparticles, made of gold nanostars and iron oxide nanospheres, as efficient therapeutic nanoheaters whose on-site delivery can be improved by magnetic targeting, is proposed. Single and combined magneto- and photo-thermal heating properties of Janus nanoparticles render them as compelling heating elements, depending on the nanoparticle dose, magnetic lobe size, and milieu conditions. In cancer cells, a much more effective effect is observed for photothermia compared to magnetic hyperthermia, while combination of the two modalities into a magneto-photothermal treatment results in a synergistic cytotoxic effect in vitro. The high potential of the Janus nanoparticles for magnetic guiding confirms them to be excellent nanostructures for in vivo magnetically enhanced photothermal therapy, leading to efficient tumor growth inhibition. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.Twelve new HLA class I alleles were characterized in the Spanish population. © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.Adipose tissue engineering aims to provide solutions to patients who require tissue reconstruction following mastectomies or other soft tissue trauma. Mesenchymal stromal cells (MSCs) robustly differentiate into the adipogenic lineage and are attractive candidates for adipose tissue engineering. This work investigates whether pore size modulates adipogenic differentiation of MSCs toward identifying optimal scaffold pore size and whether pore size modulates spatial infiltration of adipogenically differentiated cells. To assess this, extrusion-based 3D printing is used to fabricate photo-crosslinkable gelatin-based scaffolds with pore sizes in the range of 200-600 µm. The adipogenic differentiation of MSCs seeded onto these scaffolds is evaluated and robust lipid droplet formation is observed across all scaffold groups as early as after day 6 of culture. Expression of adipogenic genes on scaffolds increases significantly over time, compared to TCP controls. Furthermore, it is found that the spatial distribution of cells is dependent on the scaffold pore size, with larger pores leading to a more uniform spatial distribution of adipogenically differentiated cells. Overall, these data provide first insights into the role of scaffold pore size on MSC-based adipogenic differentiation and contribute toward the rational design of biomaterials for adipose tissue engineering in 3D volumetric spaces. © 2020 The Authors. Published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.BACKGROUND Several studies have previously demonstrated the survival benefit of both EGFR-TKI treatment and chemotherapy in patients with non-small cell lung cancer (NSCLC) harboring EGFR mutations. The aim of the present study was to clarify the factors influencing the treatment sequence after failure of EGFR-TKI therapy, focusing on the number of organs with metastasis (hereafter, metastatic organs). METHODS Between January 2010 and December 2016, consecutive patients with EGFR-mutated NSCLC who were started on first-line EGFR-TKI were reviewed. The factors influencing withholding systemic chemotherapy and the post-progression survival (PPS) after failure of EGFR-TKI were investigated. RESULTS A total of 393 patients were started on first-line EGFR-TKI during the study period. After excluding patients maintained on EGFR-TKI or who received osimertinib targeting secondary EGFR T790M, 297 patients were included in the analysis. Among these, 180 (60.6%) received chemotherapy after failure of EGFR-TKI (TKI-Ct group), while the remaining 117 (39.4%) received no chemotherapy (TKI-only group). Multivariate analysis identified older age (≥75 years odds ratio [OR] = 0.25, 95% confidence interval [CI] 0.11-0.43, P  less then  0.001), poor performance status (PS) (≥2 OR = 0.06, 95% CI 0.03-0.15, P  less then  0.001), and three or more metastatic organs (OR = 0.42, 95% CI 0.22-0.80, P = 0.008) as being significantly associated with withholding of chemotherapy after failure of EGFR-TKI. CONCLUSION A relatively large number of metastatic organs and a poor PS were associated with the withholding of subsequent chemotherapy after failure of EGFR-TKI in EGFR-mutated NSCLC patients. Further research for patients with such a poor prognosis should be investigated in the future. © 2020 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.