Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Conclusion:</b> Taken together, we proved that miR-224 might play essential roles in cellular functions of nutrient-depleted A549 cells possibly through regulating the target PTEN and downstream signal PI3K, suggesting the potential of miR-224 to be a therapeutic target for NSCLC therapy.
|
31190892 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Conclusions:</b> PI3K/Akt/HIF-1α may contribute to the progression of HPV-associated NSCLC <i>via</i> mediating the expression of EMT-related transcription factors in NSCLC cells.
|
30310502 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
36245-PHF was shown to inhibit PI3K and Aurora A and B kinases and overcome gefitinib-resistant NSCLC growth.
|
25122774 |
2014 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Non-small cell lung cancer (NSCLC) cells are often associated with constitutive activation of the phosphoinositide 3-kinase (PI3K) → Akt → mTOR pathway.
|
21421804 |
2011 |
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
NSCLC cell lines with mutant KRas-Gly12Asp had activated phosphatidylinositol 3-kinase (PI-3-K) and mitogen-activated protein/extracellular signal-regulated kinase kinase (MEK) signaling, whereas those with mutant KRas-Gly12Cys or mutant KRas-Gly12Val had activated Ral signaling and decreased growth factor-dependent Akt activation.
|
22247021 |
2012 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PI3K/Akt and MKK4/JNK pathways cooperate to stimulate NSCLC cell proliferation by maintaining cell survival, suggesting that simultaneously targeting these two pathways might be an effective therapeutic strategy against NSCLC.
|
16115952 |
2005 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
A bioinformatics technique and western blot analyses showed that the PI3K/AKT pathway is more activated in EGFR-mutated NSCLC than in MET-amplified NSCLC, and a PI3K inhibitor enhanced the sensitivity to trametinib in the EGFR-mutated cell lines, suggesting that this pathway is associated with resistance to MEK inhibitors.
|
27748834 |
2016 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
A novel PI3K/mTOR dual inhibitor XH002 exhibited robust antitumor activity in NSCLC.
|
30381967 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Aberrant phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathways play important roles and have been widely observed in the development of NSCLC.
|
20866043 |
2010 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, western blot analysis identified that CTD inhibited the phosphatidylinositol 3-kinase (PI3K)/RAC serine/threonine protein kinase (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway in NSCLC, demonstrating that the levels of phosphorylated (p-)Akt, p-mTOR, phosphorylated ribosomal p70S6 protein kinase (p-p70-S6K) and cyclin D1 were significantly decreased following treatment with CTD.
|
29731854 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Afatinib resistance in non-small cell lung cancer involves the PI3K/AKT and MAPK/ERK signalling pathways and epithelial-to-mesenchymal transition.
|
25341405 |
2015 |
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Although several groups have demonstrated that concomitant use of MEK and phosphoinositide 3-kinase (PI3K) inhibitors (MEKi/PI3Ki) can induce dramatic tumor regressions in mouse models of KRAS-mutant non-small cell lung cancer (NSCLC), ongoing clinical trials investigating this strategy have been underwhelming to date.
|
24675361 |
2014 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
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.
|
31360122 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
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.
|
31310954 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
AZD9291 promotes autophagy and inhibits PI3K/Akt pathway in NSCLC cancer cells.
|
30145802 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Blocking the PI3K pathway enhances the efficacy of ALK-targeted therapy in EML4-ALK-positive nonsmall-cell lung cancer.
|
24972969 |
2014 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
BRD4 upregulation inhibited activation of the PI3K/Akt pathway in NSCLC cells <i>in vitro</i> and <i>in vivo</i>.
|
31213835 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
By using quantitative (real-time) PCR, western blot analysis, and immunocytochemical staining, three non-small cell lung cancer (NSCLC) cell lines (A427, A549 and NCI-H358) were analyzed for the expression of EpoR and its specific downstream signaling pathways [Janus kinase 2 (Jak2)-signal transducer and activator of transcription 5 (STAT5), phosphatidylinositol-3-kinase (PI3K)-Akt, mitogen-activated protein (MAP) kinase].
|
29345289 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Clinicopathological significance of PTEN and PI3K/AKT signal transduction pathway in non-small cell lung cancer.
|
24133589 |
2013 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
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).
|
31497240 |
2019 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Compromised CCR9-CCL25 interaction promoted apoptosis in NSCLC cells by activating phosphoinositide 3-kinase (PI3K)/Akt in vitro.
|
25691296 |
2015 |
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Downregulation of miR-142-5p induced PTEN and PD-L1 protein expression and suppressed PI3K and p-Akt and protein expression in an in vitro model of NSCLC.
|
29767245 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Dual inhibition of the HSP90 and PI3K signaling pathways with sub-therapeutic doses of these combined anticancer drugs may represent a potent treatment strategy for KRAS-mutant NSCLC with intrinsic resistance to PI3K inhibition.
|
28797845 |
2017 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Dual roles of miR-374a by modulated c-Jun respectively targets CCND1-inducing PI3K/AKT signal and PTEN-suppressing Wnt/β-catenin signaling in non-small-cell lung cancer.
|
29362431 |
2018 |
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
FAM83A signaling induces epithelial-mesenchymal transition by the PI3K/AKT/Snail pathway in NSCLC.
|
31444970 |
2019 |