To summary, genes involved in cell adhesion, ECM-receptor interaction, focal adhesion, and PI3K-Akt signaling pathway play crucial roles in human lung adenocarcinomas.
MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1.
We hypothesize that activation of PP2A simultaneously inhibits the PI3K and MAPK pathways and represents a promising therapeutic strategy for the treatment of TKI-resistant LUAD.
Our current study is to identify clinical significance of minichromosome maintenance (MCM) gene expression in Lung Adenocarcinoma (LUAD) using genome-wide RNA sequencing (RNA-seq) dataset and bioinformatics analysis tools.
Further investigation identified that TSPY1 could directly bind to the promoter of insulin growth factor binding protein 3 (IGFBP3) to inhibit IGFBP3 expression and that downregulation of IGFBP3 increased the activity of PI3K/AKT/mTOR/BCL2 and RAS/RAF/MEK/ERK/JUN signaling in LUAD and LIHC cells.
We report that SIRT1 protein levels are downregulated by oncogenic K-RAS in a MEK and PI3K-dependent manner in mouse embryo fibroblasts (MEFs), and in human lung adenocarcinoma cell lines.
Therefore, we suggest that dioscin may act as a dual inhibitor of the MEK/ERK and PI3K/AKT signaling pathways to overcome TKI resistance via dysregulation of SHP2 expression in lung adenocarcinoma.
Finally, Western blot analysis was performed to measure the expressions of PI3K, p-PI3K, AKT, p-AKT, ERK1/2, p-ERK1/2, GSK3β, p-GSK3β, mTOR, and p-mTOR protein in lung adenocarcinoma and squamous cell carcinoma cells.
In addition, analysis of the copy number alterations of these 23 genes revealed correlations between <i>EMSY</i>/<i>CCND1</i>, <i>EMSY</i>/<i>PIK3CA</i>, <i>CCND1</i>/<i>CDKN2A</i>, and <i>CCND1</i>/<i>PIK3CA.</i> Our exploration of integrated copy number and gene expression analysis gives priority to the <i>PTEN</i>-<i>PIK3CA</i> and <i>RB1</i>-<i>CCND1</i> pathways in developing therapeutic strategies for LUAD patients without <i>EGFR</i> mutations or <i>ALK</i> fusion.
Disrupting the RAS-PI3K interaction inhibits activation of both AKT and RAC1 in EGFR-mutant lung cancer cells, leading to reduced growth and survival, and inhibits EGFR-mutant-induced tumor onset and promotes major regression of established tumors in an autochthonous mouse model of EGFR-mutant-induced lung adenocarcinoma.
Regulation of different components from Ophiopogon japonicus on autophagy in human lung adenocarcinoma A549Cells through PI3K/Akt/mTOR signaling pathway.
Here we report measurements of PIK3CAH1047R mutant fraction (MF) in normal colonic mucosa, normal lung, colonic adenomas, colonic adenocarcinomas, and lung adenocarcinomas.
The PI3K protein family acted as critical roles in the lung adenocarcinoma, since the components of the PI3K protein family include PIK3C2B, PIK3CA, PIK3R1 and so forth were presented in the intersections.
Pellino-1 overexpression activated PI3K/Akt and ERK signaling pathways and elicited an epithelial-mesenchymal transition (EMT) phenotype of lung adenocarcinoma cells.
The addition of PI3K-mTOR inhibitors to cisplatin or paclitaxel increased the activity of chemotherapy in the TNBC and LGSOC models; whereas no added activity was observed in the LADC model.
In conclusion, these results suggest that neferine enhances cisplatin -induced autophagic cancer cell death through downregulation of PI3K/Akt/mTOR signaling pro-survival pathway and ROS- mediated Beclin-1 and PI3K CIII independent autophagy in human lung adenocarcinoma (A549 cells).