The Subcellular Localization of IncRNA FAM230B in Osteosarcoma and Its Interaction with Early miR-203.

Previous studies have revealed the role of lncRNA FAM230B in promoting papillary thyroid cancer and gastric cancer. We predicted that FAM230B may interact with miR-203 and studied the crosstalk between FAM230B and miR-203 in osteosarcoma (OS). Paired OS and nontumor tissues donated by 60 patients with OS were subjected to RNA isolations and quantitative real-time PCR (RT-qPCR) to analyze the expression of both FAM230B and miR-203 (mature and premature levels).

MicroRNA-492 overexpression exerts suppressive effects on the progression of osteosarcoma by targeting PAK7.

MicroRNAs (miRNAs or miRs), which are a class of non-coding RNAs, have emerged as effective modulators of various aspects of biological processes. Accumulating evidence has established significant associations between the dysregulation of miRs and tumorigenesis in various types of cancer. However, the role of miR‑492, particularly in osteosarcoma (OS) remains elusive.

Beneficial effects of coculturing synovial derived mesenchymal stem cells with meniscus fibrochondrocytes are mediated by fibroblast growth factor 1: increased proliferation and collagen synthesis.

Meniscus reconstruction is in great need for orthopedic surgeons. Meniscal fibrochondrocytes transplantation was proposed to regenerate functional meniscus, with limited donor supply. We hypothesized that coculture of synovial mesenchymal stem cells (SSC) with meniscal fibrochondrocytes (me-CH) can support matrix production of me-CH, thus reducing the number of me-CH needed for meniscus reconstruction.

GDC-0152 attenuates the malignant progression of osteosarcoma promoted by ANGPTL2 via PI3K/AKT but not p38MAPK signaling pathway.

Angiopoietin-like protein 2 (ANGPTL2) plays an important role in inflammatory carcinogenesis and tumor metastasis. The compound GDC-0152 is a peptidomimetic small molecule antagonist of inhibitor of apoptosis (IAP) proteins with antitumor activity. However, the interaction between ANGPTL2 and GDC-0152 has not been studied.