Calycosin, a Phytoestrogen Isoflavone, Induces Apoptosis of Estrogen Receptor-Positive MG-63 Osteosarcoma Cells via the Phosphatidylinositol 3-Kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Pathway.
The relative protein expression level of p-PI3K, p-Akt, P53 and Bcl-2 in osteosarcoma cells after transfection with lncRNA- NC or lncRNA-LINC00628 were detected by Western blot.
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.
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.
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.
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.
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.
Overexpression of FER1L4 promotes the apoptosis and suppresses epithelial-mesenchymal transition and stemness markers via activating PI3K/AKT signaling pathway in osteosarcoma cells.
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.
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.
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.
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.