ISL could retard proliferation and promote apoptosis of U2OS cells possibly by suppressing the PI3K/Akt signalling pathway, indicating that it might be a potential therapeutic agent for osteosarcoma treatment.
Analysis of the signalling relationships of these genes, as well as other expression markers of osteosarcoma, indicated that gene networks linked to RB1, TP53, PI3K, PTEN/Akt, myc and RECQL4 are associated with osteosarcoma.
Our results indicate that TGF-α/EGFR interaction elicits PI3K and Akt activation, which in turn activates NF-κB, resulting in the expression of ICAM-1 and contributing the migration of human osteosarcoma cells.
In conclusion, the results of the present study indicated that CLDN12 promoted cell proliferation and migration through the PI3K/Akt signaling pathway in osteosarcoma cells, suggesting that CLDN12 may be a potential agent in the treatment of patients with osteosarcoma.
Our data suggest that upregulation of pro-inflammatory cytokine signal in the periaqueductal gray of cancer rats amplifies PI3K-mTOR signal in this brain region and alters the descending pathways in regulating pain transmission, and this thereby contributes to the development of bone cancer-induced pain.
We proposed that VRK1 and H2A<sup>T120ph</sup> could be the potential targets for osteosarcoma diagnosis and treatment.HighlightsH2A<sup>T120ph</sup> is specifically promoted by Ras-PI3K pathway activation.H2A<sup>T120ph</sup> joins in the oncogenic effects of Ras-PI3K pathway on osteosarcoma.H2A<sup>T120ph</sup> regulates the transcription of Ras-PI3K-targeted genes.VRK1 takes part in the regulatory function of Ras-PI3K pathway on H2A<sup>T120ph</sup>.