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.
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.
Overexpression of FER1L4 promotes the apoptosis and suppresses epithelial-mesenchymal transition and stemness markers via activating PI3K/AKT signaling pathway in osteosarcoma cells.
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.
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.
We found that hBMSC-MVs promoted U2OS cell proliferation and migration under hypoxia in vitro, and that was partially associated with the PI3K/AKT and HIF-1α pathways.
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.
Here, we have analyzed the therapeutic potential of the pan-PI3K inhibitor NVP-BKM120, which has recently entered clinical Phase II for treatment of PI3K-dependent cancers on three OS cell lines.
K-Ras<sup>G12V/Y40C</sup>-PI3K/AKT pathway regulates H1.4<sup>S35ph</sup> through PKA to promote the occurrence and development of osteosarcoma cancer.
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>.
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 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.
Our data revealed for the first time that MALAT1 increases stem cell-like properties by up-regulating RET via sponging miR-129-5p, and thus activates the PI3K-Akt signaling pathway and provides potential therapeutic targets for osteosarcoma treatment.
In conclusion, the results of the present study indicate that the expression of miRNA-21, PI3K and AKT is increased in the osteosarcoma cell line MG-63, which results in reduced expression of PTEN and increased expression of proteins in the PI3K/AKT signaling pathway, and thus increases the aggressiveness of osteosarcoma cells.