Furthermore, miR-765 was involved in tumorigenesis of OS through activating extracellular-signal-regulated kinase/ epithelial-mesenchymal transition (ERK/EMT) pathway.
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.
Delphinidin induces apoptosis and inhibits epithelial-to-mesenchymal transition via the ERK/p38 MAPK-signaling pathway in human osteosarcoma cell lines.
The results showed that miR-107 expression was upregulated in osteosarcoma tissues and cell lines. miR-107 overexpression promoted U2OS cell viability, migration, and invasion whereas it inhibited apoptosis. miR-107 inhibitor transfection ameliorated or abolished these effects after miR-107 binding to TPM1 3'-UTR-wt regulated TPM1 expression. miR-107 in U2OS cells activated MEK/ERK and NF-κB signaling pathways via TPM1.
Taken together, our data suggest that miR-143 inhibits EGFR signaling through its downstream ERK/MAPK signaling cascades to control MMP9 expression in OS.
Taken together, data show CTGF elevating MMPs expression and subsequently promoting tumor metastasis in human osteosarcoma, down-regulating miR-519d via MEK and ERK pathways, making CTGF a new molecular therapeutic target in osteosarcoma metastasis.
Phyllanthus urinaria suppresses human osteosarcoma cell invasion and migration by transcriptionally inhibiting u-PA via ERK and Akt signaling pathways.
Altogether, our data enforce the evidence of Pi as a novel signaling molecule capable of inhibiting ERK pathway and inducing sensitization to doxorubicin of osteosarcoma cells by p53-dependent apoptosis, implying that targeting Pi levels might represent a rational strategy for improving osteosarcoma therapy.