However, the precise role of T cell factors/lymphoid enhancer-binding factor (TCFs/LEF) family members, which are the major binding complex of β-catenin, in OS is poorly understood.
This is the evidence supporting the interaction between GRM4 and CBX4, which could inhibit the malignant behavior of osteosarcoma cells through the GRM4/CBX4/HIF-1α signaling pathway.
This study uncovers a novel underlying molecular mechanism of PCAT6-miR-185-5p-TGFBR1/2-TGF-β signaling axis in promoting tumor progression in OS, which indicates that PCAT6 may serve as a promising prognostic factor and therapeutic target again OS.
RIP assay, RNA pull down, and dual-luciferase reporter gene assay showed that circ_ANKIB1 could directly bind to miR-19b and act as an miR-19b sponge in osteosarcoma cells.
Taken together, our results demonstrate that dioscin can induce apoptosis through the JNK/p38 pathway and GSDME-dependent pyroptosis in OS, identifying it as a potential therapeutic drug for treatment of this disease.
To elucidate the mechanism by which miR-1225-5p inhibits the development of osteosarcoma, we identified Sox9 as a target gene of miR-1225-5p using the TargetScan website.
Circular RNA LARP4 correlates with decreased Enneking stage, better histological response, and prolonged survival profiles, and it elevates chemosensitivity to cisplatin and doxorubicin via sponging microRNA-424 in osteosarcoma.
Furthermore, the upregulation of miR-421 and downregulation of MCPIP1 resulted in poor overall survival and severe disease progression, respectively, in the patients with osteosarcoma.
In conclusion, the present study proved that LINC00324 accelerated the proliferation and migration of osteosarcoma cells through regulating WDR66, providing a new prognostic target for osteosarcoma.
Studies have indicated that Kinesin-1 light chain KLC1, Kinesin-1 heavy chain KIF5B and Kinesin-11 family motor KIF26B interact with extracellular signal-regulated kinase ERK closely to regulate neuronal differentiation and mediate the chemosensitivity of osteosarcoma cells to drugs, Kinesin-3 family motor KIF13B and Kinesin-5 family motor Eg5 perform functions in regulating p38 to regulate the myelination of nervous system and facilitate the spindle elongation and tension, Kinesin-8 family motor MS-KIF18A and three isoforms of kinesin-13 can also connect and interact with MAPK pathway to transport estrogen receptor to the nucleus and control cell migration.
Kaplan-Meier analysis indicated that overall survival of osteosarcoma patients was significantly higher in the low MCT4 expression group than in the high expression group (log-rank test, P<0.001).
SIRT6 has been reported to serve a key role in OS; chromatin‑immunoprecipitation (ChIP) and quantitative ChIP, as well as a luciferase reporter assay, demonstrated that SIRT6 was transcriptionally regulated by FOXN3.
It was found that the phosphoinositide 3‑kinase/ATK pathway was inactivated and that epithelial‑mesenchymal transition was activated in OS cell lines with overexpression of the lncRNA SNHG1.
Bioinformatics analysis suggested eIF4E would be a direct target of miR-496, and the expression of eIF4E was inhibited by overexpression of miR-496. miR-496 elevation was found to exert suppressive effects on OS cell proliferation, migration and invasion in vitro and tumor growth in vivo, with the effects being reversed using miR-496 depletion.