|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
WT1-interacting protein inhibits cell proliferation and tumorigenicity in non-small-cell lung cancer via the AKT/FOXO1 axis.
|
30690883 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We identified four (two NRAS and single AKT1 and PTEN) mutations in CNS metastases of NSCLC.
|
28097440 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We highlight the conventional mechanisms of drug resistance elicited by the complex heterogeneous microenvironment of NSCLC during targeted therapy, including mutations in epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), the receptor tyrosine kinase ROS proto-oncogene 1 (ROS1), and the serine/threonine-protein kinase BRAF (v-Raf murine sarcoma viral oncogene homolog B).
|
31715289 |
2020 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
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).
|
30496626 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
We further showed that downregulation of AKT signaling activity by using AKT inhibitor LY294002 markedly inhibited NSCLC cell proliferation and resistance to doxorubicin induced by VASH2.
|
30940294 |
2020 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
We derived <i>KRAS</i>-mutant NSCLC ganetespib-resistant cell lines to identify the resistance mechanism(s) and identified hyperactivation of RAF/MEK/ERK/RSK and PI3K/AKT/mTOR pathways as key resistance mechanisms.
|
28167505 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
We also determined the expression levels of GSK3β and p-Akt1 in patients with NSCLC and determined their potential association with survival data using Kaplan-Meier plots and CBIOTAL.
|
30832755 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
VAOS was further identified to induce NSCLC cell apoptosis through activating protein kinase B (AKT) to elevate intracellular reactive oxygen species (ROS) levels by increasing in oxygen consumption and impairing the ROS-scavenging system.
|
30223019 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Using six NSCLC cell lines, we found that the AKT-1 inhibitor, A-674563, was significantly more effective at reducing NSCLC cell survival relative to the pan-AKT inhibitor MK-2206.
|
29470540 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Using a panel of non-small cell lung cancer (NSCLC) lines, we show here that MAP-ERK kinase (MEK) and RAF inhibitors are selectively toxic for the KRAS-mutant genotype, whereas phosphoinositide 3-kinase (PI3K), AKT, and mTOR inhibitors are not.
|
23454899 |
2013 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Up or down-regulated of NOK were conducted in two NSCLC cell lines to analyze its impact on AKT/GSK3β pathway.
|
31819514 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Treatment of AKT inhibitor markedly prevented the phosphorylation of AKT and GSK3β which subsequently counteracted increasing expression of CyclinD1, CyclinE1 or Snail and restored the decreasing expression of Zo-1, as well as the upregulation of tumor proliferation and invasion, caused by ZNF452 overexpression.Taken together, the present study indicated that ZNF452 may be an upstream regulator of AKT-GSK3β signaling pathway and facilitates proliferation and invasion of NSCLC.
|
28418919 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
Together, our findings suggest that adding chloroquine to EGFR and AKT inhibition has the potential to improve tumor responses in EGFR M+ NSCLC, and that selective targeting of AKT2 may provide a new treatment option in NSCLC.
|
24946858 |
2014 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
To the best of our knowledge, the present study was the first to explore the role of miRNA-133a/epidermal growth factor receptor (EGFR) in regulating NSCLC cell growth and apoptosis via the AKT/extracellular signal-regulated kinase (ERK) signaling pathway.
|
30333876 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
To conclude, our study demonstrated that RAGE played a crucial role in the metastasis and growth of NSCLC by regulating PI3K/AKT and KRAS/RAF-1 signaling pathways, thereby might be a promising therapeutic target for NSCLC.
|
28670367 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Thus, in addition to EGFR mutations, other factors in NSCLC cells, such as high expression of ErbB family members, may constitutively activate AKT and sensitize cells to EGFR inhibitors.
|
15665299 |
2005 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study unravels an anti-metastatic role of AKT1 in the NSCLC cells with KRAS or EGFR mutations, and establishes an AKT1-MARCKS-LAMC2 feedback loop in this regulation.
|
28765579 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study aims to explore the effects of microRNA-21 (miR-21) on radiosensitivity in non-small cell lung cancer (NSCLC) by targeting programmed cell deanth 4 (PDCD4) and regulating PI3K/AKT/mTOR signaling pathway.
|
28423589 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These results thus indicate that persistent activation of signaling by the AKT-survivin pathway induced by PTEN loss underlies a mechanism of resistance to erlotinib-induced apoptosis in EGFR mutation-positive NSCLC.
|
22075159 |
2012 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results suggested that miR-548l may play a causal role through AKT1 in NSCLC invasion and metastasis.
|
25245053 |
2015 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These results suggest that the AKT1 polymorphisms could be used as prognostic markers for the patients with early-stage NSCLC.
|
21842521 |
2012 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results suggest that PTEN can up-regulate SOD, GPx and catalase activity by inhibition of PI3K/AKT pathway in NSCLC cell lines.
|
22299584 |
2013 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
These results indicate that EGFR inhibitors enhanced AdTRAIL anti-tumor activity in NSCLC cell lines and that inhibiting the AKT pathway played an important role in this enhancement.
|
21959047 |
2011 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
These findings suggested that miR‑379 acts as a tumor suppressor in NSCLC by directly targeting IGF‑1R and indirectly regulating AKT and ERK signaling pathways. miR‑379 provides novel therapeutic targets for the treatment of patients with this disease.
|
28731178 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.400 |
Biomarker
|
disease |
BEFREE |
These findings show that the FGFR1/AKT/mTOR signaling pathway plays a vital role in acquired resistance against gefitinib in NSCLC.
|
31819480 |
2019 |