Inorganic nanoparticles (INPs) have been paid great attention in the field of oncology in recent past years since they have enormous potential in drug delivery, gene delivery, photodynamic therapy (PDT), photothermal therapy (PTT), bio-imaging, driven motion, etc. To overcome the innate limitations of the conventional INPs, such as fast elimination by the immune system, low accumulation in tumor sites, and severe toxicity to the organism, great efforts have recently been made to modify naked INPs, facilitating their clinical application. Taking inspiration from nature, considerable researchers have exploited cell membrane-camouflaged INPs (CMCINPs) by coating various cell membranes onto INPs. CMCINPs naturally inherit the surface adhesive molecules, receptors, and functional proteins from the original cell membrane, making them versatile as the natural cells. In order to give a timely and representative review on this rapidly developing research subject, we highlighted recent advances in CMCINPs with superior unique merits of various INPs and natural cell membranes for cancer therapy applications. The opportunity and obstacles of CMCINPs for clinical translation were also discussed. The review is expected to assist researchers in better eliciting the effect of CMCINPs for the management of tumors and may catalyze breakthroughs in this area. Graphical Abstract

Core fucosylation catalyzed by core fucosyltransferase (Fut8) contributes to the progressions of epithelial ovarian cancer (EOC). Copper transporter 1 (CTR1), which contains one N‐glycan on Asn15, mediates cellular transport of cisplatin (cDDP), and plays an important role in the process of cDDP‐resistance in EOC. In the present study, we found that the core fucosylation level elevated significantly in the sera of cDDP‐treated EOC patients. The in vitro assays also indicate that core fucosylation of CTR1 was significantly upregulated in cDDP‐resistant A2780CP cells compared to the cDDP‐sensitive A2780S cells. Intriguingly, the hyper core fucosylation suppressed the CTR1‐cDDP interactions and cDDP‐uptake into A2780CP cells. Conversely, contrast to the Fut8+/+ mouse ovarian epithelial cells, the Fut8‐deleted (Fut8−/−) cells obviously showed higher cDDP‐uptake. Furthermore, the recovered core fucosylation induced the suppression of cDDP‐uptake in Fut8‐restored ovarian epithelial cells. In addition, the core fucosylation could regulate the phosphorylation of cDDP‐resistance‐associated molecules, such as AKT, ERK, JNK, and mTOR. Our findings suggest that the core fucosylation of CTR1 plays an important role in the cellular cDDP‐uptake and thus provide new strategies for improving the outcome of cDDP based chemotherapy of EOC.

No abstract