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MicroRNA‐128 (miR‐128) is associated with cell proliferation, differentiation, migration, apoptosis, and survival. Genetic analysis studies have demonstrated that miR‐128 participates in bone metabolism, which involves bone marrow–derived mesenchymal stem cells, osteoblasts, osteoclasts, and adipocytes. miR‐128 also participates in regeneration of skeletal muscles by targeting myoblast‐associated proteins. The deregulation of miR‐128 could lead to a series of musculoskeletal diseases. In this review, we discuss recent findings of miR‐128 in relation to bone metabolism and muscle regeneration to determine its potential therapeutic effects in musculoskeletal diseases, and to propose directions for future research in this significant field. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC), is mostly derived from normal colon epithelial cells, and has been reported to be one of most common gastrointestinal malignancies globally. An increasing number of researchers have claimed that long noncoding RNAs (lncRNAs) exert significant functions in tumor progression. Nevertheless, the function of MAGI2‐AS3 remains uncertain in CRC. The expression of MAGI2‐AS3, miR‐3163, and transmembrane protein 106B (TMEM106B) messenger RNA was examined by quantitative real‐time polymerase chain reaction. Cell apoptosis was measured by caspase‐3 activity test. Cell proliferation was tested by cell‐counting kit 8 and 5‐ethynyl‐2′‐deoxyuridine assays. Cell migration was detected by transwell assay. Western blot analysis examined the protein expression of TMEM106B. The expression of Ki‐67 was evaluated by immunohistochemistry assay. The binding capacity between miR‐3163 and MAGI2‐AS3 (or TMEM106B) was studied by radioimmunoprecipitation and luciferase reporter assays. The expression of MAGI2‐AS3 and TMEM106B was conspicuously upregulated whereas miR‐3163 presented lower expression in CRC cells. MAGI2‐AS3 deficiency facilitated cell apoptosis but hampered cell proliferation and migration. MAGI2‐AS3 combined with miR‐3163 and negatively regulated miR‐3163 expression. In addition, the administration of sh‐MAGI2‐AS3 or miR‐3163 mimics suppressed CRC cell growth in vivo. Subsequently, miR‐3163 targeted TMEM106B and the transfection of sh‐MAGI2‐AS3 or miR‐3163 mimics downregulated TMEM106B expression. Rescue assays verified that TMEM106B overexpression recovered the effects of MAGI2‐AS3 inhibition on cell apoptosis, proliferation, and migration in CRC. MAGI2‐AS3 drives CRC progression through regulating miR‐3163/TMEM106B axis. This supplies innovative insights on the investigation of molecular mechanism in CRC progression. [ABSTRACT FROM AUTHOR]

Bone metabolism is associated with many bone diseases and regulated by multiple signal pathways. Over the past three decades, the functions of a superfamily of evolutionarily conserved transcriptional regulators, known as forkhead box (Fox) family, has been demonstrated to contribute to the bone metabolism. Genetic analysis studies have demonstrated that Fox gene family participate in bone metabolism and that their expression can be regulated by multiple factors. The deregulation of Fox gene family can lead to a series of bone metabolic diseases. In this manuscript, we sketched the biology of the Foxs family, summarized its function of regulating bone metabolism and maintaining bone homeostasis to estimate its potential therapeutic effects in bone diseases, and suggested directions for future exploration in this important field. [ABSTRACT FROM AUTHOR]

The mechanistic target of rapamycin (mTOR) plays a key role in sensing and integrating large amounts of environmental cues to regulate organismal growth, homeostasis, and many major cellular processes. Recently, mounting evidences highlight its roles in regulating bone homeostasis, which sheds light on the pathogenesis of osteoporosis. The activation/inhibition of mTOR signaling is reported to positively/negatively regulate bone marrow mesenchymal stem cells (BMSCs)/osteoblasts‐mediated bone formation, adipogenic differentiation, osteocytes homeostasis, and osteoclasts‐mediated bone resorption, which result in the changes of bone homeostasis, thereby resulting in or protect against osteoporosis. Given the likely importance of mTOR signaling in the pathogenesis of osteoporosis, here we discuss the detailed mechanisms in mTOR machinery and its association with osteoporosis therapy. [ABSTRACT FROM AUTHOR]