Results show that 9 out of 10 carcinomas exhibited some degree of staining for Akt or PTEN, while normal tissue showed no staining. Akt and PTEN may be diagnostic markers for lung carcinoma.

overexpression of RRM1 in human and mouse lung cancer cell lines induced PTEN expression, reduced phosphorylation of focal adhesion kinase (FAK), suppressed migration, invasion, and metastasis formation, and increased survival in an animal model.

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

PTEN could be a good prognostic factor for lung carcinomas, regardless of the histological types.

Up-regulation of PTEN at the transcriptional level is an advers prognostic factor in female lung adenocarcinomas.

Western blot analysis showed that six out of 25 (24%) lung cancer cell lines displayed low expression of PTEN protein.

Report expression of FAK and PTEN in bronchioloalveolar carcinoma and lung adenocarcinoma.

p16INK4A, DAPK1, PTEN and MT1G genes were not frequently methylated in the stage I non-small cell lung cancer in China.

Hypermethylation of PTEN was significantly associated with shorter time to recurrence of nonsmall cell lung cancer.

promoter methylation is not an important mechanism for PTEN deregulation in non-small-cell lung cancers (NSCLCs) from Koreans.

Compared with their parental cells, the expressions of CDA, RRM1, PTEN and ERCC1 increase in human gemcitabine-resistant non-small cell lung cancer cell lines.

PTEN instability-mediated constitutive Akt activation is involved in acquired resistance mechanisms to cetuximab and also induces de novo resistance to gefitinib in non-small cell lung cancer cells.

mutations in PTEN is associated with squamous cell carcinomas of the lung.

loss of PTEN expression contributes to gefitinib and erlotinib resistance in non-small cell lung cancer.

Relevance of the combinatorial inactivation of PTEN in non-small cell lung carcinoma progession.

augments invasiveness and growth of lung cancer cells through the PI3K/AKT/NFkB pathway

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 non-small cell lung cancer.

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.

PTEN up-regulates superoxide dismutase, glutathione peroxidase and catalase activity by inhibition of PI3K/AKT pathway in non-small cell lung cancer cell lines.

aberrant p16 alterations directly correlated with altered those in PTEN in non-small cell 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

The tumorigenic role of miR-21 in non-small cell lung cancer development through modulation of the PTEN signaling pathway.

Loss of phosphatase and tensin homolog protein expression is associated with lung adenocarcinoma.

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.

Vandetanib might be effective in non small cell lung carcinoma with EGFR mutations that lack PTEN expression.

Low PTEN expression is associated with malignant phenotypes in non-small cell lung cancer.

Our results demonstrated that miR-205 is involved in the tumorigenesis of Non-small cell lung cancer through modulation of the PTEN signaling pathway.

this study further extends the biological role of miR-92b in non-small cell lung cancer A549 cells and for the first time identifies PTEN as a novel target of miR-92b.

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.

PTEN loss was greater in lung squamous cell carcinomas than in adenocarcinom

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

Study reveals a critical role for the PTEN/PI3K pathway in both SCLC and lung adenocarcinoma.

The presence of individual and multiple alterations of p53, p16 and PTEN were compared in in non-small cell lung carcinoma (NSCLC), glioma and breast carcinoma.

Results show that up-regulation of miR-21 and down-regulation of Pten in patients with non-small cell lung cancer negatively correlate with shorter disease-free survival and poor sensitivity to treatment with tyrosine kinase inhibitors.

lung cancer patients with Oct4 high, PTEN low and TNC high expression profile significantly correlated with poor disease-free survival

Combined detection of PTEN and miR-494 can aid in determining malignancy degree and the prognosis of patients with non-small cell lung cancer

Data shows that PTEN protein is expressed in both nucleus and cytosol of lung neuroendocrine tumors (NET) and suggests that cellular ubiquitinylation and sumoylation likely influence the functional PTEN loss in high grade lung NETs.

PTEN is a direct target of MIR205 in lung cancer tissue. MIR205 might inhibit lung cancer cell proliferation by regulating PTEN expression.

High levels of PTEN expression pointed to a favorable prognostic marker in non-small cell lung cancer.

MiRNA-10a is upregulated in non-small cell lung carcinoma and activates PTEN/AKT/ERK pathway.

a decrease in PTEN facilitates ROS/SHP2 signaling, causing lung cancer cells to become unresponsive to IFN-gamma

Among advanced lung adenocarcinoma patients treated with platinum-based chemotherapy, the carriers of homozygous PTEN SNPS rs701848 and rs11202592 had significantly worse overall survival than heterozygotes or wild-type homozygotes, especially in stage III. Haplotype analysis revealed a protective effect of the haplotype G-A-A (in the order of rs11202592, rs701848, and rs11202607) on chemotherapy efficacy and survival.

Reduced PTEN expression may be an indicator for poor prognosis in patients with lung cancer. The presence of PTEN expression may define a subset of patients with lung cancer appropriate for investigational therapeutic strategies

decreased expression of PTEN correlated with poor overall survival in non-small cell lung cancer patients and was indicative of a poor prognosis for disease-free survival and progression-free survival in patients with NSCLC [review and meta-analysis]

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

Case Report: multiple primary lung cancer displaying heterogeneous EGFR and PTEN molecular profiles. The right lung lesion displayed gefitinib-insensitivity and the lesions in the left lung were gefitinib-sensitive.

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

Our results demonstrate that NEDD4 may promote the acquired resistance of non-small-cell lung cancer cells to erlotinib by decreasing phosphatase and tensin homolog deleted on chromosome 10 protein expression. Targeted decrease in NEDD4 expression may be a potential therapeutic strategy for tyrosine kinase inhibitor-resistant non-small-cell lung cancer.

The aim of this review is to shed light on the role of four different phosphatases (PTEN, PP2A, CDC25 and DUSP1) in five different solid tumors (breast cancer, lung cancer, pancreatic cancer, prostate cancer and ovarian cancer), in order to better understand the most frequent and aggressive primary cancer of the central nervous system, glioblastoma.

High PTEN expression is associated with Non-Small Cell lung cancer.

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.

CK1alpha bound the C-terminal tail of PTEN and enhanced both PTEN stability and activity by competitively antagonizing NEDD4-1-induced PTEN polyubiquitination and abrogating PTEN phosphorylation, thereby inhibiting AKT activity and activating FOXO3a-induced transcription of Atg7, to suppress lung tumor growth.

The inhibition of PTEN also reduced the cancer effects of CD4+ T cells on non-small cell lung cancer (NSCLC) cell lines following miR-142-5p downregulation. Therefore, our study demonstrated that miR-142-5p regulated CD4+ T cells in human NSCLC through PD-L1 expression via the PTEN pathway.

MiR-221 together with proteins MDR1 and ABCG2 was upregulated in Cisplatin-resistant A549 lung cancer cells. Anti-miR-221 inhibits proliferation and induces senescence in lung cancer cells. PTEN/Akt pathway axis was identified as a target of drug resistance induced by miR-221.

The results implied that both squamous and glandular components of adenosquamous carcinoma of the lung may share the same oncogenic driver pathway for carcinogenesis, which is reflected in the patterns of expression of PTEN and PD-L1.

We identified that PTEN loss and increased MET copy number may predict an unfavorable survival in mutated-EGFR non-small-cell lung cancer patients.

These results indicated that LINC00702 modulated the expression of PTEN gene by acting as a ceRNA for miR-510 in non-small cell lung cancer.

tis study shows that PTEN inactivation induces epithelial-mesenchymal transition and metastasis by intranuclear translocation of beta-catenin and snail/slug in non-small cell lung carcinoma cells

KRAS exon 3 and PTEN exon 7 mutations had no significant impact on overall survival of small-cell lung cancer patients.

CELF2 suppresses non-small cell lung carcinoma growth by inhibiting the PREX2-PTEN interaction.

miR-4262 enhances Paclitaxel (PTX) resistance in non-small cell lung cancer (NSCLC) cells through targeting PTEN and activating the PI3 K/Akt signalling pathway. The inhibition of miR-4262 expression might be an improved treatment to overcome PTX resistance in NSCLC.

PLCE1 inhibits apoptosis of non-small cell lung cancer via promoting PTEN methylation.

LncRNA MAGI2-AS3 suppresses the proliferation and invasion of non-small cell lung carcinoma through miRNA-23a-3p/PTEN axis.

PTEN loss activates a functional AKT/CXCR4 signaling axis to potentiate tumor growth and lung metastasis in human osteosarcoma cells.

FOXF2 aggravates the progression of non-small cell lung cancer through targeting lncRNA H19 to downregulate PTEN.

serum exosomal miR-106b level was significantly increased in lung cancer patients and positively associated with TNM stages and lymph node metastasis. Furthermore, exosomal miR-106b enhanced the migrated and invasive ability of lung cancer cells by regulating PTEN.

LINC-PINT alleviates lung cancer progression via sponging miR-543 and inducing PTEN.

Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression.

The long noncoding RNA CASC7 inhibits growth and invasion of nonsmall cell lung cancer cells through phosphatase and tensin homolog upregulation via sequestration of miR92a.

Long noncoding RNA MEG3 inhibits cell migration and invasion of nonsmall cell lung cancer cells by regulating the miR215p/PTEN axis.

that overexpression of RRM1 in human and mouse lung cancer cell lines induced PTEN expression, reduced phosphorylation of focal adhesion kinase (FAK), suppressed migration, invasion, and metastasis formation, and increased survival in an animal model.

Pten is essential for both normal lung morphogenesis and the prevention of lung carcinogenesis, possibly because this tumor suppressor is required for bronchioalveolar stem cells homeostasis.

Pten inactivation cooperated with oncogenic K-ras in promoting lung tumorigenesis.

Loss of one or both PTEN alleles resulted in a dramatic acceleration of mammary tumor onset and an increased occurrence of lung metastases in the ErbB-2(KI) strain.

The deletion of a single copy of Pten does not substantially add to the lung tumor phenotype conferred by mutation of K-ras by NNK, and there is likely no selective advantage for loss of the second Pten allele in lung tumor initiation.

mutations are relatively common in non-small cell lung cancers

That PTEN deletion does not increase lung squamous cell carcinoma formation compared to Kras(G12D) activation.

biallelic inactivation of Lkb1 and Pten in the mouse lung leads to lung squamous cell carcinoma that recapitulates the histology, gene expression, and microenvironment found in human disease.

Genomic analysis identifies deregulated PTEN signaling as a driver of murine Small Cell lung Carcinoma progression.

Ras induction of ZEB1 is required for tumour initiation in a lung adenocarcinoma model via Pten repression. A lower threshold of ZEB1 is sufficient for cancer initiation, whereas further induction is necessary for tumour metastasis.

The WAP-Cre:Pten(f/f):p53(lox.stop.lox_R270H) mice develop basal-like breast cancer that is enriched in TICs, can readily form lung metastasis, and provides a preclinical model to study both basal-like and claudin-low TNBC in immune-competent mice.