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The aim of this study was to provide a new effective carrier for rescuing the sensitivity of drug‐resistant in breast cancer cells. Nano‐gold micelles loaded with Dox and Elacridar (FP‐ssD@A‐E) were chemically synthesised. With the increase in the amount of Dox and Elacridar, the encapsulation rate of FP‐ssD@A‐E gradually increased, and the drug loading rate gradually decreased. FP‐ss@A‐E had a sustained‐release effect. Dox, Elacridar, FP‐ss@AuNPs, and FP‐ssD@A‐E significantly improved cell apoptosis, in which, FP‐ssD@A‐E was the most significant. FP‐ssD@A‐E significantly decreased the cell viability and improved the Dox uptake. The levels of VEGFR‐1, P‐gp, IL‐6, and i‐NOS were significantly decreased after Dox, Dox + Elacridar, FP‐ss@AuNPs, and FP‐ssD@A‐E treatment. It was worth noting that FP‐ssD@A‐E had the most significant effects. The prepared FP‐ssD@A‐E micelles, which were spherical in shape, uniform in particle size distribution, and had good drug loading performance and encapsulation efficiency. [ABSTRACT FROM AUTHOR]

Background: Downregulation of KAI1 gene expression has been found in many types of cancer cells and is closely related to cancer invasion and metastasis. This study was aimed at investigating the effects and possible underlying mechanisms of KAI1 gene on invasion and metastasis of human hepatocellular carcinoma (HCC). Methods: The invasive ability, visco-elastic properties and cell adhesion forces were analysed in different HCC cells originating from the MHCC97-H cell line transfected with either the sense or the antisense KAI1 expression plasmid. Tumuorigenicity, metastatic abilities, extracellular matrix (ECM) and intercellular adhesion molecule-1 (ICAM-1) expression were also evaluated in the nude mouse models of the xenografted and orthotopic liver cancer cells. Results: Compared with their parental cells, in the HCC cells transfected with the sense KAI1 gene, the invasive ability in vitro was significantly decreased ( P<0.01); the cellular elastic coefficients K1, K2 and μ were significantly higher ( P<0.05); the cells adhesion forces to fibronectin were significantly lower ( P<0.01). The sense KAI1 gene transfection into the cancer cells also inhibited their invasion and lung metastasis in the orthotopic liver cancer nude mice. However, the opposite changes were observed in the HCC cells transfected with the antisense KAI1 gene. KAI1 gene transfection also affected ECM and ICAM-1 expression in the transplanted liver cancer. Conclusion: The KAI1 gene plays an important role in the invasion and metastasis of human HCC and its upregulation in HCC cells suppresses their invasive and metastatic abilities. KAI1 gene functioned as a metastasis inhibitor by regulating the HCC cell biophysical behaviours including aggregation, adhesion, motility and visco-elastic properties. [ABSTRACT FROM AUTHOR]