EGF and hypoxia induce CXCR4 in non-small cell lung cancer, a process regulated by the PI3-kinase/PTEN/AKT/mTOR signaling pathway and activation of HIF-1alpha

Results describe the roles of MEK1/ERK and AKT/PKB pathways on the effects of granulocyte macrophage colony-stimulating factor (GM-CSF) and M-CSF on tumor progression of lung cancer.

AKT amplification and the mTOR/p70S6K1 pathway play an important role in human lung cancer cells acquiring CDDP resistance

These data provide evidence that, although AKT1 mutations are apparently rare in lung cancer (1.9%), the oncogenic properties of E17K-AKT1 may contribute to the development of a fraction of lung carcinoma with squamous histotype (5.5%).

Prognostic and/or predictive role of Akt phosphorylation in breast, prostate and non-small cell lung cancer. Review.

The effect of AKT1 on DNA-dependent protein kinase catalytic subunit (DNA-PKcs) activity and DNA-dsb repair in irradiated non-small cell lung cancer cell lines A549 and H460, was analysed.

The lack of Par-4 dramatically enhances Ras-induced lung carcinoma formation in vivo, acting as a negative regulator of Akt activation.

results suggest that CCL5 acts through PI3K/Akt, which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activation of alphavbeta3 integrin and contributing to the migration of human lung cancer cells

KAI1/CD82 decreased the metastatic phenotype of H1299 lung carcinoma cells by down-regulating Rac1 expression through the PI3K/Akt/mTOR pathway.

periostin promoted the survival of A549 non-small-cell lung cancer cells under hypoxic microenvironment via activation of Akt/PKB pathway

These results established a novel pathway that consists of proto-oncogene c-Akt, COX-2 and Mcl-1 for acquired apoptosis resistance in lung cancer cells.

ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB

AKT1-SNP4 A/A genotype seems to be a candidate biomarker of primary resistance in non-small lung cancer patient treated with gefitinib.

Thermo-chemotherapy has a stronger inhibitory effect than chemotherapy alone in lung tumor cell growth, probably through induction of ROS production and subsequent inhibition of Akt pathway activation and Caspase pathway-induced cancer cell apoptosis.

cIAP2 upregulated by E6 via EGFR/PI3K/AKT cascades may contribute to cisplatin resistance, revealing that the EGFR or PI3K inhibitor combined with cisplatin may improve the chemotherapeutic efficacy in HPV-infected lung cancer.

Constitutive activation of EGFR/Akt/mTOR pathway was present in defined subset of nonsmall cell lung carcinomas.

elevated Id1 expression was observed in lung cancer cell lines as well as lung cancer tissues. Id1 overexpression increased cell proliferation while Id1 knockdown decreased cell proliferation, mostly through Akt-related pathway

Angiopoietin-2, an angiogenic regulator, promotes initial growth and survival of breast cancer metastases to the lung through the integrin-linked kinase (ILK)-AKT1,2-B cell lymphoma 2 (Bcl-2) pathway.

Our data demonstrate that Akt1 and notably Akt3 regulate proliferation, survival, migration and epidermal growth factor-mediated signal transduction in non small cell lung cancer-derived disseminated tumor cells

AKT1 polymorphisms are associated with early stage non-small cell lung cancer.

Overexpression of MUC1 enhances proangiogenic activity of non-small-cell lung cancer cells through activation of Akt and extracellular signal-regulated kinase pathways.

Akt/mTOR might be effective targets to overcome the resistance to IGF-1R mAbs in head and neck squamous cell carcinoma and non-small cell lung carcinomas.

analysis of AKT signaling pathway activated by HIN-1 methylation in non-small cell lung cancer

EphB3 suppresses non-small-cell lung cancer metastasis via a PP2A/RACK1/Akt signalling complex

Overexpression of mu-opioid receptor has a possible direct affect on Akt and mTOR activation and lung cancer progression.

The relationship between expression and genetic alterations of the components of the PI3K/AKT pathway in non-small cell lung cancer, was investigated.

a novel USP1-PHLPP1-Akt signaling axis, and decreased USP1 level in lung cancer cells may play an important role in lung cancer progress.

expression of pAkt and mTOR expression is more significantly associated with adenocarcinoma than squamous cell carcinomaof the lung

amplification of AKT1 and/or AKT2 and high-level polysomy were found in 16% of total lung carcinoma cases, and this defined subset was characterized by the overexpression/activation of Akt, reciprocal to EGFR aberrations.

AKT1 rs2494752 polymorphism is associated with treatment response in advanced non-small cell lung cancer.

Data show that miR-7 inhibits the effects of TLR9 signaling on lung cancer cells through regulation of the PIK3R3/Akt pathway.

Data show that a photodynamic therapy (PDT) dose-dependent upregulation of CRP gene, as well as of PTX3 and ficolin 1 genes in lung tumor A549 cells, and indicate critical role played by PI3K/Akt/AP-1 pathway.

Data indicate that the PTEN loss and activation of AKT signaling pathway contributed to erlotinib resistance in EGFR-mutant non-small cell lung cancer (NSCLC) cell line H1650.

We found that AKT activation in serum-deprived conditions is not common among lung cancer cell lines and correlates with activating mutation in either EGFR or PIK3CA, loss of PTEN, or amplification of ERBB2

epigenetic downregulation of RUNX3 can induce docetaxel resistance in human lung adenocarcinoma cells by activating AKT signaling.

activation of RAF1-MEK1-ERK/AKT axis may determine the resistance of non-small cell lung cancer cell lines bearing wild type EGFR to erlotinib

Orai3 constitutes a native store-operated calcium entry pathway in non small cell lung adenocarcinoma that controls cell proliferation and cell cycle progression, likely via Akt pathway.

Found progressive loss of PTEN and increase in EGFR, TGF-alpha, P-AKT expression from benign samples to non small cell lung cancer. Changes were correlated to differentiation extent of cancer tissue, metastasis of lymph nodes and histological classification.

IWS1, an RNA processing regulator, is phosphorylated by Akt3 and Akt1 at Ser720/Thr721 in lung cancer

mutations may confer resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in lung adenocarcinoma patients

sensitivity of lung cancer cells to miR-153 is determined by its endogenous miR-153 level

RBP2 promotes HIF-1alpha-VEGF-induced angiogenesis of non-small cell lung cancer via the Akt pathway.

High AKT1 expression is associated with lymph node metastasis of non-small cell lung cancer.

signalings can reciprocally and positively regulate each other, leading to enhanced non-small cell lung cancer (NSCLC) cell proliferation and survival.

knockdown of PTX3 suppressed tumor proliferation and invasion of lung adenocarcinoma cells, followed by decreased expression of p-AKT, p-NF-kappa B, PCNA, and MMP-9

this study is the first to demonstrate that HG treatment of A549 human lung epithelial cells promotes tumor cell invasion and increases metastasis-associated protein expression by up-regulating HO-1 expression via ROS or the TGF-1/PI3K/Akt signaling

Akt and phosphoinositide 3-kinase pathway activation plays role in suppressing apoptosis of non-small cell lung cancer cells.

Data show that cytoplasmic cyclin-dependent kinase inhibitor p27 is preferentially observed in primary non-small cell lung cancer (NSCLC) with activated proto-oncogene proteins c-akt1 and predicts poor survival.

CRISPR-Cas9n-mediated knockout and reconstitution studies establish that dynamin-1 is activated by Akt/GSK3beta signaling in H1299 non-small lung cancer cells.

Reciprocal positive regulation between Cx26 and PI3K/Akt pathway confers acquired gefitinib resistance in non-small-cell lung carcinoma cells by promoting epithelial mesenchymal transition via a gap-junctional communication-independent manner.

Inactivated Sendai virus induces apoptosis and autophagy via the PI3K/Akt/mTOR/p70S6K pathway in human non-small cell lung cancer cells.

MicroRNA-31 inhibits lung adenocarcinoma stem-like cells via down-regulation of MET-PI3K-Akt signaling pathway

these data suggest that DHA-induced apoptosis and autophagy in non-small cell lung cancer cells are associated with AMPK activation and PI3K/Akt inhibition, which in turn lead to suppression of mTOR

MiR-185 acts as a tumor suppressor by targeting AKT1 in non-small cell lung cancer cells.

Study of four cases confirms BRAF V600E mutation as a probable driver in a subset of ciliated muconodular papillary tumors (CMPT) of the lung, along with AKT1 mutation, which further supports that CMPT are indolent pulmonary neoplasms.

Our study revealed genomic differences between pulmonary sclerosing hemangioma (PSH) and lung adenocarcinomas, including a high rate of AKT1 mutation in PSHs. These genomic features of PSH identified in the present study provide clues to understanding the biology of PSH and for differential genomic diagnosis of lung tumors

IL-24 inhibits AKT via regulating the HMGA1/miR-222 signaling node in human lung cancer cells and acts as an effective tumor suppressor.

High expression of AKT1 is associated with invasion in non-small cell lung cancer.

PTEN downregulates the PI3K/AKT/hTERT pathway, thereby suppressing the growth of lung adenocarcinoma cells.

In conclusion, baicalin and DDP were synergistic at inhibiting proliferation and invasion of human lung cancer cells at appropriate dosages and incubation time in the presence or absence of DDP resistance. The attenuation of DDP resistance was associated with downregulation of MARK2 and p-Akt.

suggest that the reduction of CLDN5, 7, and 18 expression loses the suppressive ability of interaction between PDK1 and Akt and causes sustained phosphorylation of Akt, resulting in the disordered proliferation in lung squamous carcinoma cells

High AKT1 expression is associated with lung cancer.

Data show while overexpression of AKT serine/threonine kinase 1 (AKT1) promoted local tumor growth, downregulation of AKT1 or overexpression of AKT serine/threonine kinase 2 (AKT2) promoted peritumoral invasion and lung metastasis.

our study found that intracellular Ca(2+) could promote radioresistance of non-small cell lung cancer cells through phosphorylating of Akt on the 473 site, which contributes to a better understanding on the non-small cell lung cancer radioresistance, and may provide a new target for radioresistance management

results suggest that Kctd20 impacts proliferation and invasion of non-small cell lung cancer through enhancing Fak and Akt phosphorylation

ong non-coding RNA ROR may affect the sensitivity of lung adenocarcinoma cells to DDP by targeting PI3K/Akt/mTOR signaling pathway

AKT inhibition blocks miR-124 silencing-induced AKT1/2, glucose transporter 1, hexokinase II activation, cell proliferation, and glycolytic or energy metabolism changes. In summary, this study demonstrated that miR-124 is able to inhibit proliferation, glycolysis, and energy metabolism, potentially by targeting AKT1/2-glucose transporter 1/hexokinase II in non-small cell lung cancer cells.

High AKT1 expression is associated with non-small cell lung cancer metastasis.

reduction of Alex3 correlates with the development of non-small cell lung cancer and predicts adverse clinical outcome of non-small cell lung cancer patients. The effect of Alex3 on inhibiting invasion and migration may attribute to upregulation of E-cadherin expression through AKT-Slug pathway inactivation.

The findings indicated that miR-135a promotes cell apoptosis and inhibits cell proliferation, migration, invasion and tumor angiogenesis by targeting IGF-1 gene through the IGF-1/PI3K/Akt signaling pathway in non-small cell lung cancer.

High AKT1 expression is associated with lung cancer.

Visfatin increases the nuclear translocation of Akt and its binding with ABCC1. These data showed that visfatin can decrease doxorubicin sensitivity of Non-small-cell lung cancer cells via activation of Akt/MRP1.

Data show that LINC00963 (MetaLnc9) interacted with the glycolytic kinase PGK1 and prevented its ubiquitination in non-small cell lung cancer (NSCLC) cells, leading to activation of the oncogenic AKT/mTOR signaling pathway.

Low Frequency Magnetic Fields Induce Autophagy-associated Cell Death in lung cancer through miR-486-mediated Inhibition of Akt/mTOR Signaling pathway.

High AKT1 expression is associated with drug resistance in non-small cell lung cancer.

the results indicated that JB inhibits glycolysis by down-regulating HK2 expression through inactivating the Akt/mTOR pathway in non-small cell lung cancer (NSCLC) cells, suggesting that JB might be a potential therapeutic agent for the treatment of NSCLC.

Study shows that the lack of Akt1 in human lung endothelial cells promotes prostate cancer cell transendothelial migration in vitro and metastasis to the mouse lungs in vivo involving increased nuclear localisation of beta-catenin and suppression of endothelial tight-junction proteins.

results demonstrated that PLAUR induces geftinib-resistance through EGFR/p-AKT/survivin signaling pathway in gefitinib-resistant human lung adenocarcinoma cells. PLAUR could be a novel therapeutic target for gefitinib-resistant NSCLC patients.

High AKT1 expression is associated with tumor-node-metastasis in nonsmall cell lung cancer.

miR-1179 inhibits the growth and invasion of non-small cell lung cancer cells by targeting SPAG5 and inhibiting Akt

miR-935 is down-regulated in non-small cell lung cancer tissue, is linked to poor outcome, and acts on signal transduction mediator E2F7 and the AKT pathway.

APE1 stimulates EGFR-tyrosine kinase inhibitors resistance by activating Akt signaling through a redox-dependent mechanism in lung adenocarcinoma.

High AKT1 expression is associated with lung cancer.

LncRNA TP73-AS1 promoted the progression of lung adenocarcinoma via PI3K/AKT pathway.

High expressions of AKT1 is associated with non-small cell lung cancer.

USP49 inhibits non-small cell lung cancer cell growth by suppressing PIK3R2/AKT signaling.

the data of the present study support that miR3383p inhibits lung cancer cell invasion and proliferation by downregulating AKT/bcatenin signaling pathway. The present findings supported the potential use of miR3383p in the treatment of lung cancer

NFIA enhances cell radiosensitivity by downregulating p-AKT and p-ERK in non-small cell lung cancer

we revealed that CPA4 downregulation may induce apoptosis and G1-S arrest by suppressing the protein kinase B/c-MYC pathway. These results suggest that CPA4 has an oncogenic effect on lung cancer growth. Taken together, we identified a novel gene in lung cancer that might provide a basis for new therapeutic targets.

NUSAP1 knockdown inhibits cell growth and metastasis of non-small-cell lung cancer through regulating BTG2/PI3K/Akt signaling.

PRMT5 Promotes Human lung cancer Cell Apoptosis via Akt/Gsk3beta Signaling Induced by Resveratrol.

MAGI1-IT1 stimulates proliferation in non-small cell lung cancer by upregulating AKT1 as a ceRNA.

overexpression of (phosphorylated)p-Akt, p-mTOR and p-eIF4E proteins is associated with metastasis and poor prognosis of non-small cell lung cancer patients.

USP53 promotes apoptosis and inhibits glycolysis in lung adenocarcinoma through FKBP51-AKT1 signaling.

Given that Akt inhibitors in clinical development as cancer therapeutics are not isoform selective, these studies support specific targeting of Akt1 to mitigate the effects of mutant K-ras in lung cancer

Our study demonstrated that miR-26a enhanced lung cancer cell metastasis potential via modulation of metastasis-related gene expression, and activation of AKT pathway by PTEN suppression

study shows that adjacent tumors cohabiting the same lung can have differential AKT activities and sensitivities to dietary restriction, despite Pten loss

Dual expression of shAkt1 and Pdcd4 effectively suppresses lung tumorigenesis.

High Akt1 enhanced lung tumor development.

Data show that Akt/mTOR and MAPK pathways were activated in ovine pulmonary adenocarcinoma (OPA) lung and envelope (Env) of Jaagsiekte sheep retrovirus (JSRV) transfected NIH 3T3 cells.

Zi Shen Decoction Inhibits Growth and Metastasis of lung cancer via Regulating the AKT/GSK-3beta/beta-Catenin pathway.