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

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.

These results pinpoint mTOR as a mechanism of resistance to chemotherapy in KRAS-mutant lung cancer and validate a rational and readily translatable strategy that combines mTOR inhibitors with standard chemotherapy to treat KRAS-mutant adenocarcinoma, the most common and deadliest lung cancer subset.

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

one rational approach for mTOR-targeted lung cancer therapy is to use an mTOR inhibitor in combination with a drug that blocks PI3K/Akt activation such as a PI3K inhibitor, as we demonstrated in our study.21

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

mTOR expression defines a subgroup of patients with a favorable outcome and may be useful for prognostic stratification of lung adenocarcinoma patients as well as incorporation of mTOR into clinical decisions.

Overexpression of the mammalian target of rapamycin is associated with non-small cell lung cancer.

EphA2 mutation in lung squamous cell carcinoma promotes increased cell survival, cell invasion, focal adhesions, and mammalian target of rapamycin activation

Inhibition of the mTOR signal may be a promising strategy for radiosensitization with no relevance to p53 gene status from the aspects of lung cancer cell lethality and cell growth depression.

these data demonstrate a differential mTOR activation status in the spectrum of pulmonary neuroendocrine tumors, possibly suggesting that mTOR pathway profiling might play a predictive role in candidate patients for mTOR-targeted therapies.

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

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.

The absence of and/or a low expression of PTEN and activated mTOR may play an important role in the development of non-small cell lung cancer.

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

In non-small cell lung cancer cells, LKB1/AMPK signaling negatively regulates mTOR activity and contributes to cell growth inhibition in response to energy stress.

High phosphorylated mTOR expression is associated with non- small cell lung cancer.

Data indicate that responses were noted in patients with HER2-amplified breast cancer resistant to trastuzumab, HER2-mutant non-small-cell lung cancer, and tumor types without identified mutations in the HER-PI3K-mTOR pathway.

A feedback inhibition loop of mTORC1 onto mTORC2 plays a role in the homeostasis of E-cadherin expression in lung cancer cells.

miR-99a/mTOR pathway was involved in diaporine A-induced tumor suppression in non-small cell lung cancer cells.

mTOR complex 2 regulates cell survival and growth in non-small-cell lung cancer (NSCLC) cell lines by stabilizing Mcl1.

investigated the involvement of the RAS/MEK/ERK and PI3K/AKT/mammalian target of rapamycin (mTOR) pathways on metabolic alteration in lung adenocarcinoma cell lines with activating EGFR mutations

This result indicates that p-mTOR might play a more pivotal role in the biologic behavior of early small cell lung cancers than advanced ones

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

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

mRNA expression of BIM and MTOR in 57 patients with EGFR-mutant non-small-cell lung cancer.

our results show for the first time that KPNA2 is transcriptionally and post-translationally regulated by the mTOR pathway and provide new insights into targeted therapy for non-small cell lung cancer

Describe a novel interaction between Rheb and the tumor suppressor RASSF1A. This interaction may allow coordinate upregulation of Hippo while TOR is suppressed to modulate the balance of apoptosis and autophagy in lung tumor cells.

Activation of the PI3K/mTOR pathway following PARP Inhibition in Small Cell lung cancer.

non-small cell lung cancer savolitinib resistance arises via multiple mechanisms that converge on MET-independent mTOR and MYC activation

dual PI3K and mTOR inhibitor, BEZ235 with the HDAC inhibitor Trichostatin A (TSA) significantly increased anti-tumor activities compared with BEZ235 and TSA alone, suggesting a combination treatment for non-small-cell lung cancer (NSCLC).

Report outcome of PIK3CA/mTOR/MEK co-targeted inhibition strategy in the treatment of non-small cell lung carcinomas.

High expression of mTOR is associated with lung cancer.

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

Results show that mTOR expression level is dowregulated in non-small cell lung cancer (NSCLC) and that its protein phosphylation level is down when NSCLC cells are transfected with miR-145.

High mTOR expression is associated with lung cancer.

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.

Long non-coding RNA DANCR contributes to lung adenocarcinoma progression by sponging miR-496 to modulate mTOR expression.

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.

miR33a5p inhibited the proliferation of lung adenocarcinoma cells, enhanced the antitumor effect of celastrol, and improved sensitivity to celastrol by targeting mTOR in lung adenocarcinoma in vitro and in vivo

miR-181 may be a novel and important regulator of cisplatin-resistant non-small cell lung cancer by serving a role in the regulation of apoptosis, as an established rate-limiting miRNA target.

Taken together, the present study provides the first evidence that OTUB2 acts as a pivotal driver in non-small cell lung cancer tumorigenesis by stabilizing U2AF2 and activating the AKT/mTOR pathway and the Warburg effect.

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.

Enhanced autocrine FGF19/FGFR4 signaling drives the progression of lung squamous cell carcinoma, which responds to mTOR inhibitor AZD2104.

Down-regulation of long non-coding RNA DUXAP8 suppresses proliferation, metastasis and EMT by modulating miR-498 through TRIM44-mediated AKT/mTOR pathway in non-small-cell lung cancer.

MicroRNA-365 inhibits the progression of lung adenocarcinoma through targeting ETS1 and inactivating AKT/mTOR pathway.