Nectin-4 was overexpressed at all stages of metastasis and angiogenesis, thus appearing to play a major role in tumor relapse through the PI3K-Akt-NFκβ pathway.
In this study, we aimed to investigate the effects of combined treatment with Notch1 signaling blocker DAPT and PI3K/Akt signal blocker LY294002 on metastasis of gastric cancer.
High GNAS expression showed a close correlation with a reduced overall survival (p = 0.021), frequent distal metastasis (p = 0.026), advanced clinical stage (p = 0.001), stronger cell proliferation (ki67<sup>+</sup> positive cell rate, p = 0.0351) and enhanced cancer cell migration, which was further confirmed by in vitro and in vivo assays and might be dependent on the PI3K/AKT/Snail1/E-cadherin axis.
More excitingly, the nanoregulator-reshaped TIME is effectively reserved due to the synergistic effect of hypoxia alleviation and MDSC PI3Kγ inhibition, leading to remarkable post-medication inhibition of tumor re-growth and metastasis in an animal study.
Cells treated with BCP, in a dose-dependent manner, exhibited morphological changes, showed lower cell growth, underwent apoptosis and lost the ability to metastasis through the suppression of NF-ҡ B via PI3K/AKT signalling pathway.
Coadministration of chemotherapy and PI3K/Akt pathway treatment with multistage acidity/CathB enzyme-responsive nanocarriers for inhibiting the metastasis of breast cancer.
Hsa_circ_0067934 is overexpressed and plays an oncogenic role in GBM by promoting cancer cell proliferation and metastasis via upregulation of PI3K-AKT pathway, which suggests that hsa_circ_0067934 is likely to serve as an efficient therapeutic approach in respect of GBM treatment.
STAT3-induced upregulation of lncRNA SNHG17 predicts a poor prognosis of melanoma and promotes cell proliferation and metastasis through regulating PI3K-AKT pathway.
The aims of this study were to develop original mouse models of patient-derived primary GC orthotopic xenografts (PDOX) allowing the development of distant metastases as preclinical models to study the anti-metastatic efficiency of drugs such as the phosphatidylinositol 3-kinase (PI3K) inhibitor Buparlisib (BKM120).
Pharmacologic inhibition of BRD4 using JQ1 and/or PI3K using dual PI3K/BRD4 inhibitor SF2523 (previously reported by our group as a potent inhibitor to block tumor growth and metastasis in various cancer models) suppresses tumor growth in syngeneic and spontaneous murine cancer models; reduces infiltration of myeloid-derived suppressor cells; blocks polarization of immunosuppressive MΘs; restores CD8<sup>+</sup> T-cell activity; and stimulates antitumor immune responses.