mir-21-5p inhibits the progression of human chondrosarcoma by regulating CCR7/STAT3/NF-κB pathway.

: MicroRNAs (miRNAs or miRs) play an important role in the initiation and development of chondrosarcoma (CS). However, the role of miR-21-5p in CS progression and its underlying molecular mechanisms remains unclear.: miR-21-5p expression was measured by qRT-PCR.

HSP90 regulates osteosarcoma cell apoptosis by targeting the p53/TCF-1-mediated transcriptional network.

Osteosarcoma (OS) is the most common bone tumor that occurs predominantly in children and teenagers. Although many genes, such as p53 and Rb1, have been shown to be mutated, deregulation of the canonical Wnt/β-catenin signaling pathway is frequently observed in OS. We recently demonstrated that heat shock protein 90 (HSP90) is involved in the regulation of runt-related transcription factor 2 via the AKT/GSK-3β/β-catenin signaling pathway in OS.

Atomic Force Microscopy-Based Nanoscopy of Chondrogenically Differentiating Human Adipose-Derived Stem Cells: Nanostructure and Integrin β1 Expression.

Integrin β1 is known to be involved in differentiation, migration, proliferation, wound repair, tissue development, and organogenesis. In order to analyze the binding probability between integrin β1 ligand and cluster of differentiation 29 (CD29) receptors, atomic force microscopy (AFM) was used to detect native integrin β1-coupled receptors on the surface of human adipose-derived stem cells (hADSc). The binding probability of integrin β1 ligand-receptor interaction was probed by integrin β1-functionalized tips on hADSc during early chondrogenic differentiation at the two-dimensional cell culture level.

Transcriptional regulation of Runx2 by HSP90 controls osteosarcoma apoptosis via the AKT/GSK-3β/β-catenin signaling.

Osteosarcoma (OS) is the most malignant primary bone tumor in children and adolescents with limited treatment options and poor prognosis. Recently, aberrant expression of Runx2 has been found in OS, thereby contributing to the development, and progression of OS. However, the upstream signaling molecules that regulate its expression in OS remain largely unknown.

Slug signaling is up-regulated by CCL21/CCR7 [corrected] to induce EMT in human chondrosarcoma.

In recent decades, the CXC chemokine receptor 7 (CCR7) [corrected] and its ligand CCL21 have been extensively reported to be associated with tumorigenesis. Meanwhile, Slug signaling induces the epithelial-mesenchymal transition (EMT) process in chondrosarcoma development. In the present study, we explored the functions of CCL21/CCR7 [corrected] in Slug-mediated EMT in the chondrosarcoma.