Epidermal Growth Factor Receptor Gene Mutation Status in Primary Lung Adenocarcinoma and Corresponding Bone Metastases.

Background: The aim of this study was to compare epidermal growth factor receptor (EGFR) mutations between primary tumors and corresponding bone metastases (BMs) in lung adenocarcinoma.

Materials And Methods: In total, 115 paired primary lung adenocarcinoma and corresponding BM tumors were analyzed for EGFR mutations by Amplification Refractory Mutation System.

Results: EGFR mutations were detected in 61 primary lung adenocarcinomas (53.

Comparison of Epidermal Growth Factor Receptor Gene Mutations Identified Using Pleural Effusion and Primary Tumor Tissue Samples in Non-Small Cell Lung Cancer.

Background: Although the use of pleural effusion samples for epidermal growth factor receptor (EGFR) testing in lung cancer is increasing, the accuracy rate and effectiveness of identifying EGFR mutations using these samples, rather than primary tumor tissue samples, is not established.

Materials And Methods: One hundred ninety-two advanced, non-small cell lung cancer patients were enrolled into this study. All patients had primary tumor tissue and corresponding pleural effusion samples, and we employed the Amplification Refractory Mutation System to detect EGFR gene mutations in these samples.

The Expression Pattern of p120-Catenin is Associated With Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non-Small Cell Lung Cancer.

Background: Previous research connects p120-catenin (p120ctn) with epidermal growth factor receptor (EGFR) signaling pathways, which presents a potential role for p120ctn in EGFR tyrosine kinase inhibitor (EGFR-TKIs) resistance. However, a direct correlation between the expression pattern of p120ctn in solid tumors and the therapeutic effect of EGFR-TKIs has not yet been demonstrated.

Methods And Results: In this study, the expression pattern of p120ctn was examined in patients with the EGFR gene mutation in lung adenocarcinoma, and p120ctn was found to have different patterns of expression even in the same mutation type.

The P21-activated kinase expression pattern is different in non-small cell lung cancer and affects lung cancer cell sensitivity to epidermal growth factor receptor tyrosine kinase inhibitors.

Exploring methods for increasing epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) sensitivity has become a major focus in non-small cell lung cancer (NSCLC). Major downstream effectors of the Rho family small guanosine triphosphatases, P21-activated kinases (PAKs) activate the main signaling pathways downstream of EGFR and thus promote tumor cell proliferation. In this study, we explored the expression pattern of phosphorylated PAKs in NSCLC and their potential value as drug targets for treating cancer.

Kaiso interacts with p120-catenin to regulate β-catenin expression at the transcriptional level.

Background: We have reported that p120-catenin could regulate β-catenin transcription in lung cancer cells, but the specific mechanism is unclear.

Methods And Results: In this study, bisulfite sequencing PCR showed that the β-catenin promoter region in SPC-A-1 and LTEP-a-2 lung cancer cell lines has Kaiso binding sites sequences and CpG islands which may combine with Kaiso. The demethylating reagent 5-Aza-2'-deoxycytidine significantly upregulated β-catenin mRNA expression in lung cancer cell lines, whereas expression was significantly reduced following transfection with Kaiso.

Abnormal expression of Pygopus 2 correlates with a malignant phenotype in human lung cancer.

Background: Pygopus 2 (Pygo2) is a Pygo family member and an important component of the Wnt signaling transcriptional complex. Despite this data, no clinical studies investigating Pygo2 expression in lung cancer have yet been reported.

Methods: In the present study, the expression patterns of Pygo2 were evaluated by immunochemistry in 168 patients with non-small cell lung cancer (NSCLC).

Ataxia-telangiectasia group D complementing gene (ATDC) promotes lung cancer cell proliferation by activating NF-κB pathway.

Previous studies suggested Ataxia-telangiectasia group D complementing gene (ATDC) as an oncogene in many types of cancer. However, its expression and biological functions in non-small cell lung cancer (NSCLC) remain unclear. Herein, we investigated its expression pattern in 109 cases of human NSCLC samples by immunohistochemistry and found that ATDC was overexpressed in 62 of 109 NSCLC samples (56.

Leucine zipper tumor suppressor 2 inhibits cell proliferation and regulates Lef/Tcf-dependent transcription through Akt/GSK3β signaling pathway in lung cancer.

Leucine zipper tumor suppressor 2 (LZTS2) is implicated in several cancers; however, its biological mechanisms in non-small cell lung cancer (NSCLC) are not yet understood. We found that low levels of LZTS2 in NSCLC were correlated with tumor and nodal status. LZTS2 could inhibit cell proliferation and cell cycle transition at the G1/S phase and was implicated in the regulation of proteins associated with the canonical Wnt pathway, including GSK3β and β-catenin through inactivating the Akt pathway.

Ataxia-telangiectasia group D complementing gene (ATDC) upregulates matrix metalloproteinase 9 (MMP-9) to promote lung cancer cell invasion by activating ERK and JNK pathways.

Although the expression pattern and biological functions of ataxia-telangiectasia group D complementing gene (ATDC) had been implicated in several types of cancer, the roles and potential mechanisms of ATDC in lung cancer cell invasion are still ambiguous. In this study, we used gain- and loss-of-function analyses to explore the roles and potential mechanisms of ATDC in lung cancer cell invasion. siRNA knockdown of ATDC impaired cell invasion in A549 and H1299 cell lines, and its overexpression promoted cell invasion in HBE cell line.

Derlin-1 is overexpressed in non-small cell lung cancer and promotes cancer cell invasion via EGFR-ERK-mediated up-regulation of MMP-2 and MMP-9.

Previous studies indicated a role of Derlin-1 in human cancers; however, its expression pattern in non-small cell lung cancer (NSCLC) and the molecular mechanism of Derlin-1 on cancer progression have not been characterized. In the present study, Derlin-1 expression was examined in lung cancer cell lines and human tissues. Derlin-1 overexpression correlated with pTNM stage, lymph node metastasis, and poor overall survival.

Overexpression of CRKL correlates with poor prognosis and cell proliferation in non-small cell lung cancer.

Crk-Like (CRKL) is an adapter protein that has crucial roles in multiple biological processes, including cell proliferation, adhesion, and migration. Amplification of CRKL gene was found in non-small cell lung cancer (NSCLC). However, the expression pattern of CRKL protein and its clinical significance in human NSCLC have not been well characterized to date.

CIP2A is overexpressed in non-small cell lung cancer and correlates with poor prognosis.

Background: Cancerous inhibitor of protein phosphatase 2A (CIP2A) is an oncoprotein inhibiting proteolytic degradation of c-MYC. In this study, we investigated the clinical relevance of CIP2A in NSCLC.

Materials And Methods: We analyzed CIP2A mRNA expression in 29 NSCLC tissues using quantitative reverse transcription polymerase chain reaction (RT-QPCR).

delta-Catenin promotes malignant phenotype of non-small cell lung cancer by non-competitive binding to E-cadherin with p120ctn in cytoplasm.

As a member of the catenin family, little is known about the clinical significance and possible mechanism of delta-catenin expression in numerous tumours. We examined the expression of delta-catenin by immunohistochemistry in 115 cases of non-small cell lung cancer (NSCLC) (including 65 cases with follow-up records and 50 cases with paired lymph node metastasis lesions). The mRNA and protein expression of delta-catenin was also detected in 30 cases of paired lung cancer tissues and normal lung tissues by RT-PCR and western blotting, respectively.

Overexpression of SCC-S2 correlates with lymph node metastasis and poor prognosis in patients with non-small-cell lung cancer.

The objective of the current study was to investigate the expression pattern and clinicopathological significance of SCC-S2 in patients with non-small-cell lung cancer (NSCLC). The expression profile of SCC-S2 in NSCLC tissues and adjacent noncancerous lung tissues was detected by real-time RT-PCR, western blot analysis, and immunohistochemistry. In 25 lung cancer tissues examined, 18 (72%) of them exhibited stronger levels of SCC-S2 mRNA compared with their corresponding normal tissues.

Axin downregulates TCF-4 transcription via beta-catenin, but not p53, and inhibits the proliferation and invasion of lung cancer cells.

Background: We previously reported that overexpression of Axin downregulates T cell factor-4 (TCF-4) transcription. However, the mechanism(s) by which Axin downregulates the transcription and expression of TCF-4 is not clear. It has been reported that beta-catenin promotes and p53 inhibits TCF-4 transcription, respectively.

Ablation of p120-catenin enhances invasion and metastasis of human lung cancer cells.

p120-catenin, a member of the Armadillo gene family, has emerged as both a master regulator of cadherin stability and an important modulator of small GTPase activities. Therefore, it plays novel roles in tumor malignant phenotype, such as invasion and metastasis. We have reported previously that abnormal expression of p120-catenin is associated with lymph node metastasis in lung squamous cell carcinomas (SCC) and adenocarcinomas.

P120-catenin isoforms 1A and 3A differently affect invasion and proliferation of lung cancer cells.

Different isoforms of p120-catenin (p120ctn), a member of the Armadillo gene family, are variably expressed in different tissues as a result of alternative splicing and the use of multiple translation initiation codons. When expressed in cancer cells, these isoforms may confer different properties with respect to cell adhesion and invasion. We have previously reported that the p120ctn isoforms 1 and 3 were the most highly expressed isoforms in normal lung tissues, and their expression level was reduced in lung tumor cells.

Dishevelled family proteins are expressed in non-small cell lung cancer and function differentially on tumor progression.

Background: Dishevelled (Dvl) family proteins are cytoplasmic mediators of the Wnt/beta-catenin signaling pathway and have recently been linked to cancers. However, the roles of individual Dvls and their expression in human cancers are poorly defined. This work aimed to characterize the expression of Dvls and their correlation to clinicopathological factors and beta-catenin expression in non-small cell lung cancer (NSCLC).