Although the role of EGFR in PI3K/Akt signaling cascade in NSCLC is extensively studied, the molecular link between EGFR and p53 and the role of ROS in pathogenesis of NSCLC are limitedly addressed.
These data suggest that cardamonin suppressed NSCLC cell proliferation and inhibited metastasis partly by restraining the PI3K/Akt/mTOR pathway and it might be an effective therapeutic compound for NSCLC in the future.
Further analyses identified an integrin β3-mediated ternary complex comprising NRP1-integrin β3-KRAS<sup>MUT</sup> and its downstream signaling of PI3K-Akt and RalB-TBK1 as a primary resistance mechanism of KRAS<sup>MUT</sup> NSCLC to cetuximab treatment.
However, there is a lack of information about the ability of PolyI:C to affect PI3K/Akt/p53 signaling pathway in non-small cell lung cancer (NSCLC), and its pharmacodynamic evaluation in vivo still remain unclear so far.
The present study investigated the effects of a PI3K inhibitor on NSCLC growth in bone and osteoclast formation, and aimed to determine whether it could control symptoms associated with bone metastasis.
We have conducted this study to check the effect of VCN-2 on the cell viability and the effect on PTEN (Phosphatase and tensin homolog), PI3KCA (Phosphatidylinositol 4, 5-biphosphate 3-kinase catalytic subunit alpha isoform/PI3K 110α subunit), and Akt1 when VCN-2 was used alone and in combination with radiation in the NSCLC cell line NCI-H23 (H23).
The present findings suggested that treatment with pemetrexed may exhibit synergistic effects with PTEN on lung cancer cells via the inhibition of the PI3K/AKT/mTOR signaling pathway and through carbohydrate metabolism, and treatment with pemetrexed combined with PTEN overexpression may represent a novel therapeutic strategy for the treatment of NSCLC.
An effective drug sensitizing agent increases gefitinib treatment by down regulating PI3K/Akt/mTOR pathway and up regulating autophagy in non-small cell lung cancer.
The phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT), MEK/ERK pathway and TGF‑β are targets of NSCLC drugs that are already approved or are currently under investigation.
Collectively, our results, both <i>in vivo</i> and <i>in vitro</i>, demonstrate that BBD leads to autophagic cell death through downregulating the PI3K/AKT/mTOR signaling pathway and improved the antitumor effects of cisplatin in non-small cell lung cancer (NSCLC).
Notably, miR‑802 was able to deactivate the phosphoinositide 3‑kinase (PI3K)/AKT serine/threonine kinase (Akt)/mammalian target of rapamycin (mTOR) pathway in NSCLC cells in vitro and in vivo.
Low levels of IFNγ endowed cancer stem-like properties via the intercellular adhesion molecule-1 (ICAM1)-PI3K-Akt-Notch1 axis, whereas high levels of IFNγ activated the JAK1-STAT1-caspase pathway to induce apoptosis in non-small cell lung cancer (NSCLC).
We assessed whether buparlisib, a class 1 PI3K inhibitor, can be safely combined with radiotherapy in patients with non-small cell lung carcinoma (NSCLC) and investigated its effect on tumour hypoxia.