MiR‐329 has been proved to be a tumor suppressor gene in various malignancies, however, its role in osteosarcoma remains elusive. We found that miR‐329 is remarkably downregulated in osteosarcoma tissues and relates to advanced stages. MiR‐329 is able to inhibit osteosarcoma cell proliferation, promote apoptosis, and induce G0/G1 cell cycle arrest. In addition, miR‐329 also suppresses wound‐healing and migration ability of osteosarcoma cells and inhibits tumorigenicity in vivo. Rab10 was identified as a target of miR‐329 in osteosarcoma and mediates its biofunction. These findings may shed light to the understanding of tumor development in osteosarcoma.

Supplemental Digital Content is available in the text

The coassembly of block copolymers (BCPs) with nanoscale inorganic objects is an important route to fabricate nanostructured polymer composites. However, the immiscibility of inorganic/polymeric interface is a recurring challenge to overcome, particularly for inorganic clusters, such as the polyoxometalates (POMs)/BCPs system. In this paper, we present a general method to incorporate POMs into BCP matrices, in which a POM cluster is embedded as a core in a supramolecular star polymer (SSP) whose arms possess the same chemical composition as a BCP segment. Because of the enthalpic interaction between SSP arms and BCP segments, the SSP can carry POM into BCP matrices to realize their coassembly. By this way, we successfully localize a Keggin-type POM cluster [CoW 12 O 40 ] 6− modified with polystyrene (PS) arms into the PS domain of poly(styrene-b-ethylene oxide) micelles, which induces the formation of a series of hybrid micelles with spherical, toroidal, and bicontinuous structures. The morphological transition of micelles can be adjusted by the length of PS arms and the content of cluster cores. The mechanism is studied by both experimental methods and simulations. An unconventional mechanism for toroid formation is disclosed for the first time, which follows a sphere− rosary−toroid pathway. Furthermore, the electrostatically bonded structure of SSP is found to play a crucial role on this pathway. These results not only pave the way for fabricating cluster−polymer nanocomposites with controllable structures but also provide new insights into comprehending the self-assembly behavior of complex polymer systems.

Supplemental Digital Content is available in the text

No abstract

No abstract

No abstract

Osteosarcoma (OS), the most common bone cancer, causes high morbidity in children and youngadults. TRIM46 is a member of the family of tripartite motif (TRIM)-containing proteins that serve asimportant regulators of tumorigenesis. Here, we investigate the possible role of TRIM46 in OS andthe underlying molecular mechanism. We report an increase in the expression of TRIM46 in OS andits association with tumor size, Enneking’s stage, and patient prognosis. TRIM46 knockdown inhibitsOS cell viability and cell cycle progression and induces apoptosis, while TRIM46 overexpression exertsinverse effects, which are inhibited by peroxisome proliferator-activated receptor alpha (PPARα)overexpression and the nuclear factor kappa B (NF-κB) inhibitor, pyrrolidine dithiocarbamate (PDTC).Furthermore, TRIM46 negatively regulates PPAR expression via ubiquitination-mediated proteindegradation and modification. PPAR overexpression also inactivates NF-κB signaling and NF-κBpromoter activity in OS cells overexpressing TRIM46. Moreover, TRIM46 knockdown inhibits tumorgrowth and induces apoptosis of OS cells in vivo. TRIM46 acts as an oncogene in OS by interactingwith and ubiquitinating PPARα, resulting in the activation of NF-κB signaling pathway. Thus, TRIM46may be a potential biomarker of carcinogenesis.