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CoCrFeNiMn high-entropy alloy (HEA) has great potential for engineering application due to its good ductility and high fracture toughness at low temperature. It can be deposited on components as coatings to take advantage of its excellent properties and reduce the cost. In this study, CoCrFeNiMn HEA coatings were deposited on 316L stainless steel substrates by atmospheric plasma spraying (APS) technique, and a series of transient thermal shock tests were performed. It was found that the coatings contained two main phases: a face-centered cubic (FCC) solid solution phase and a flocculent oxides phase. The elemental contents of Co, Cr, Fe, and Ni were close to equal atomic percentage in the coating, while Mn was reduced significantly. The oxygen was mainly distributed in the dark flocculent oxides phase. After transient thermal shock tests, these two phases remained stable, but some tiny cracks appeared on the surface. Meanwhile, the microhardness of the coating after transient thermal shock tests also showed stable, ∼ 420 HV. Weibull statistics were used to analyze the reliability of the microhardness, and the Weibull modulus m was distributed from 9 to 15. The CoCrFeNiMn HEA coating exhibited high phase stability and excellent properties under transient thermal shock, making it have service advantages in extreme environments, especially in the fields of the development of future nuclear and aerospace structural materials.

FAM83A (family with sequence similarity 83, member A) has been found to be highly expressed in cancers. The purpose of this study was to clarify the role and mechanism of FAM83A in lung cancers. The expression of FAM83A in lung cancer cells was enhanced by gene transfection or knocked down by small interfering RNA interference. The key proteins of the Wnt signaling pathway, the Hippo signaling pathway, and epithelial–mesenchymal transition (EMT) were examined using Western blot. The proliferation and invasion of lung cancer cells were examined using cell proliferation, colony formation, and invasion assays. The expression of FAM83A in lung cancer tissues was significantly increased and was correlated with advanced tumor–node–metastasis (TNM) stage and poor prognosis. Overexpression of FAM83A enhanced the proliferation, colony formation, and invasion of lung cancer cells. Meanwhile, FAM83A overexpression increased the expression of active β-catenin and Wnt target genes and the activity of EMT. Furthermore, in FAM83A-overexpressed cells, the activity of Hippo pathway was downregulated, whereas the expression of yes-associated protein (YAP) and its downstream targets cyclin E and CTGF were upregulated. The inhibitor of the Wnt signaling pathway, XAV-939, reversed the promoting effect of FAM83A on YAP, cyclin E, and CTGF. On knocking down the expression of FAM83A, we obtained the opposite results. However, the inhibitor of GSK3β, CHIR-99021, restored the expression of YAP, cyclin E, and CTGF after FAM83A was knocked down. FAM83A is highly expressed in lung cancers and correlated with advanced TNM stage and poor prognosis. FAM83A promotes the proliferation and invasion of lung cancer cells by regulating the Wnt and Hippo signaling pathways and EMT process.