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Photothermal therapy (PTT) is a rapidly developing approach for cancer therapy, which has been widely recognized to exert high efficacy as compared to chemotherapy. However, the limited tumour homing property of currently available drug delivery systems (DDSs) is the bottleneck for the efficient delivery of photothermal agents. Here in this study, we surface modified silica nanoparticles (SLN) with the cell membrane (CM) derived from 143B cells to construct a platform (CM/SLN) capable of targeting the homogenous 143B cells. In addition, indocyanine green (ICG) as a photothermal agent was encapsulated into CM/SLN to finally construct a DDS suitable for tumour-targeted PTT of osteosarcoma. Our results revealed that CM/SLN/ICG was mono-dispersed core-shell nanoparticles with advanced stability in a physiological environment. Moreover, due to the modification of CM, CM/SLN/ICG could specifically target the homogenous 143B cells both in vitro and in vivo, which demonstrated superior anticancer efficacy when compared with either SLN/ICG or free ICG. Hence, CM/SLN/ICG could be a promising DDS for tumour targeted PTT of osteosarcoma.

Background: Osteosarcoma (OS) is one of the most common types of primary bone tumors which poses negative effects on the bones of both young children and adolescents. LncRNA LINC00472 has been reported to be involved with poor prognostics in breast cancer and ovarian cancer. As a new lncRNA, its role in OS remains to be elusive. Herein, we are focused to explore its regulatory mechanism in the development of OS. Methods: qRT-PCR was utilized to examine the expressions of LINC00472 and miR-300 in OS tissues and cell lines. OS cell lines of U2OS and MG63 were used to investigate the biological function of LINC00472. Xenograft tumor model was built in nude mice with MG63 cells. Results: The expressions of LINC00472 were inhibited in OS tissues and cells, and were negatively related to the expressions of miR-300. LINC00472 directly targeted miR-300. FOXO1 was inhibited in OS tissues and its expressions were negatively related to the expressions of miR-300. LINC00472 over-expressions decreased cell proliferation abilities and colony formation abilities. These effects were mediated by miR-300. The silence of LINC00472 and overexpressions of miR-300 suppressed FOXO1 expressions. LINC00472 greatly reduced tumor growth in vivo and this effect was attenuated by miR-300 mimic. Conclusions: From all the experiments and observations, we demonstrated that LINC00472 could be a potential tumor suppressor in OS through interacting with miR-300 and FOXO1.