DOX-doped MOF nanoparticles were prepared via a one-pot reaction and successively anchored with Fe3+ and HA for simultaneous targeted drug delivery and MR imaging.
Human bone demonstrates superior mechanical properties due to its sophisticated hierarchical architecture spanning from the nano/microscopic level to the macroscopic. Bone grafts are in high demand due to the rising number of surgeries because of increasing incidence of orthopedic disorders, non‐union fractures, and injuries in the geriatric population. The bone scaffolds need to provide porous matrix with interconnected porosity for tissue growth as well as sufficient strength to withstand physiological loads, and be compatible with physiological remodeling by osteoclasts/osteoblasts. The‐state‐of‐art additive manufacturing (AM) technologies for bone tissue engineering enable the manipulation of gross geometries, for example, they rely on the gaps between printed materials to create interconnected pores in 3D scaffolds. Herein, the authors firstly print hierarchical and porous hydroxyapatite (HAP) structures with interconnected pores to mimic human bones from microscopic (below 10 µm) to macroscopic (submillimeter to millimeter level) by combining freeze casting and extrusion‐based 3D printing. The compression test of 3D printed scaffold demonstrates superior compressive stress (22 MPa) and strain (4.4%). The human mesenchymal stromal cells (MSCs) tests demonstrate the biocompatibility of printed scaffold.
Background More and more studies have shown that circular RNAs (circRNAs) play a critical regulatory role in many cancers. However, the potential molecular mechanism of circRNAs in prostate cancer (PCa) remains largely unknown. Methods Differentially expressed circRNAs were identified by RNA sequencing. The expression of hsa_circ_0003258 was evaluated using quantitative real-time PCR and RNA in situ hybridization. The impacts of hsa_circ_0003258 on the metastasis of PCa cells were investigated by a series of in vitro and in vivo assays. Lastly, the underlying mechanism of hsa_circ_0003258 was revealed by Western blot, biotin-labeled RNA pulldown, RNA immunoprecipitation, luciferase assays and rescue experiments. Results Increased expression of hsa_circ_0003258 was found in PCa tissues and was associated with advanced TNM stage and ISUP grade. Overexpression of hsa_circ_0003258 promoted PCa cell migration by inducing epithelial mesenchymal transformation (EMT) in vitro as well as tumor metastasis in vivo, while knockdown of hsa_circ_0003258 exerts the opposite effect. Mechanistically, hsa_circ_0003258 could elevate the expression of Rho GTPase activating protein 5 (ARHGAP5) via sponging miR-653-5p. In addition, hsa_circ_0003258 physically binds to insulin like growth factor 2 mRNA binding protein 3 (IGF2BP3) in the cytoplasm and enhanced HDAC4 mRNA stability, in which it activates ERK signalling pathway, then triggers EMT programming and finally accelerates the metastasis of PCa. Conclusions Upregulation of hsa_circ_0003258 drives tumor progression through both hsa_circ_0003258/miR-653-5p/ARHGAP5 axis and hsa_circ_0003258/IGF2BP3 /HDAC4 axis. Hsa_circ_0003258 may act as a promising biomarker for metastasis of PCa and an attractive target for PCa intervention.
miRNAs play critical role in the development and progression of prostate cancer. Here we studied the role of miR-618 in prostate cancer migration and invasion. miR-618 was downregulated in metastatic androgen-independent prostate cancer (AIPC), patients with low miR-618 had poor outcome. Overexpression of miR-618 inhibited migration and invasion and induced mesenchymal to epithelial transition (MET). Conversely, knockdown of miR-618 promoted migration and invasion and induced epithelial to mesenchymal transition (EMT). FOXP2 was the direct target of miR-618, and promoted TGF-β expression, inhibition of TGF-β reversed the effect of miR-618 knockdown. We further analyzed the correlation between miR-618 expression and FOXP2 in human prostate cancer tissues, and found there was a negative correlation between miR-618 expression and FOXP2 levels. In conclusion, we found miR-618 inhibited prostate cancer migration and invasion by targeting FOXP2 and inhibiting TGF-β.
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