Functional analysis suggests that these lncRNAs were related to the PI3K-Akt signaling pathway, the Wnt signaling pathway, and the G-protein coupled receptor signaling pathway, all of which have various, important roles in osteosarcoma development.
Our data first reported that DBH-AS1 may act as an oncogenic lncRNA by modulating the PI3K/Akt pathway in osteosarcoma, which may serve as a candidate prognostic biomarker and target for new therapies in osteosarcoma.
Therefore, the current study reveals that aclidinium bromide might inhibit osteosarcoma cell growth by regulating the PI3K/AKT signaling pathway, which suggests aclidinium bromide is a potential chemotherapeutic agent for osteosarcoma.
In addition, exogenous IGF‑1R expression abolished the tumor suppressive roles of miR‑939 in OS cells. miR‑939 was implicated in the deactivation of the PI3K/Akt pathway in OS in vitro and in vivo through regulating IGF‑1R expression.
Moreover, <i>UCA1</i> increases CREB1 expression by functioning as a ceRNA against miR-582, thus promoting the EMT process via CREB1-mediated PI3K/AKT/mTOR pathway and finally leading to osteosarcoma metastasis.
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 results demonstrated that addition of SNA to anti-PD1 significantly altered infiltration and function of innate immune cells, providing the rationale for combination therapy in patients with osteosarcoma through inhibiting the function of MDSCs with a selective PI3Kδ/γ inhibitor to enhance responses to immune checkpoint blockade.
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>.