Recently, biomimetic nanoparticles for tumor−targeted therapy have attracted intensifying interest. Although exosomes are an excellent biomimetic material, numerous challenges are still hindering its clinical applications, such as low yield, insufficient targeting efficiency, and high cost. In this work, urinary exosomes (UEs) with high expression of CD9 and CD47 were extracted from breast cancer patients by a non−invasive method. Here, a nanotechnology approach is reported for tumor homologous targeting via CD9 and phagocytosis escape via CD47 through UE−coated poly (2−ethyl−2−oxazoline)−poly (D, L−lactide) (PEOz−PLA) nanoparticles (UEPP NPs). The cytotoxic agent doxorubicin (DOX)−loaded UEPP (UEPP−D) NPs with an initial particle size of 61.5 nm showed a burst release under acidic condition mimicking the tumor microenvironment. In vitro experiments revealed that UEPP−D NPs exhibited significantly improved cellular uptake, cytotoxicity, and apoptosis in MCF−7 cell lines as compared to DOX−loaded PEOz−PLA nanoparticles (PP−D NPs) and free DOX. More importantly, anti−phagocytosis and pharmacokinetic studies confirmed that UEPP−D NPs had superior immune escape ability and significantly prolonged the drug’s bloodstream circulation in vivo. Finally, UEPP−D NPs showed a markedly higher antitumor efficacy and lower side−toxicity in MCF−7 tumor bearing nude mice model. Thus, this versatile nano−system with immune escape, homologous targeting, and rapid response release characteristics could be a promising tool for breast cancer treatment.

Background: Long noncoding RNAs (lncRNAs) have been proved to be an important regulator in gene expression. In almost all kinds of cancers, lncRNAs participated in the process of pathogenesis, invasion, and metastasis. Meanwhile, compared with the large amounts of patients, there is rare knowledge about the role of lncRNAs in prostate cancer (PCa). Material/Method: In this study, lncRNA expression profiles of prostate cancer were detected by Agilent microarray chip, 5 pairs of case and control specimens were involved in. Differentially expressed lncRNAs were screened out by volcano plot for constructing lncRNA-miRNA-mRNA central network. Then, the top ten up-regulated and down-regulated lncRNAs were validated by qRT-PCR in another 5 tumor specimens and 7 para-cancerous/benign contrasts. Furthermore, we searched for the survival curve of the top 10 upregulated and downregulated lncRNAs. Results: A total of 817 differentially expressed lncRNAs were filtered out by the criteria of fold change (FC) and t-test p < 0.05. Among them, 422 were upregulated, whereas 395 were downregulated in PCa tissues. Gene ontology and KEGG pathway analyses showed that many lncRNAs were implicated in carcinogenesis. lnc-MYL2-4:1 (FC = 0.00141, p = 0.01909) and NR_125857 (FC = 59.27658, p = 0.00128) had the highest magnitude of change. The subsequent qPCR confirmed the expression of NR_125857 was in accordance with the clinical samples. High expression of PCA3, PCAT14 and AP001610.9 led to high hazard ratio while low expression of RP11-279F6.2 led to high hazard ratio. Conclusions: Our study detected a relatively novel complicated map of lncRNAs in PCa, which may have the potential to investigate for diagnosis, treatment and follow-up in PCa. Our study revealed the expression of NR_125857 in human PCa tissues was most up-regulated. Further studies are needed to investigate to figure out the mechanisms in PCa.

Background Non‐small cell lung cancer (NSCLC) is one of the most prevalent and severe malignant tumors in the world and its molecular mechanism is still unclear. In recent years, increasing evidence indicates the significant roles of circRNAs in NSCLC. It has been determined that 2‐methoxyestradiol (2‐MeOE2) exerts antitumor roles in many cancers. However, the molecular mechanism of 2‐MeOE2 in regulating the development of lung cancer needs further elucidation. Methods The expression levels of circ_0010235, microRNA‐34a‐5p (miR‐34a‐5p), and nuclear factor of activated T cells 5 (NFAT5) were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR). Cell proliferation, apoptosis and invasion were detected by cell counting kit‐8 (CCK‐8), 5‐ethynyl‐2′‐deoxyuridine (EdU) assay, flow cytometry and transwell assays, respectively. The interaction between miR‐34a‐5p and circ_0010235 or NFAT5 was predicted by bioinformatic software and confirmed by dual‐luciferase reporter assay. Results Our data showed 2‐MeOE2 hindered cell proliferation, invasion and induced apoptosis in NSCLC, which could be reversed by upregulation of circ_0010235 and NFAT5 or miR‐34a‐5p knockdown. Circ_0010235 and NFAT5 expression levels were increased, and miR‐34a‐5p expression level was decreased in NSCLC tissues and cells. In addition, 2‐MeOE2 treatment suppressed the expression of circ_0010235 and NFAT5 while promoted the expression of miR‐34a‐5p. Furthermore, circ_0010235 functioned as a molecular sponge of miR‐34a‐5p to regulate NFAT5 expression. Knockdown of circ_0010235 or 2‐MeOE2 treatment constrained tumor growth in vivo, and circ_0010235 depletion enhanced the inhibitory effect of 2‐MeOE2 on tumor growth in vivo. Conclusion These findings demonstrated that 2‐MeOE2 retarded NSCLC progression by modulating the circ_0010235/miR‐34a‐5p/NFAT5 axis, thus providing a new perspective for 2‐MeOE2 treatment in NSCLC.