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Background and objective Heat shock protein 90 kDa alpha, class B member 1 (Hsp90AB1) is highly conserved ATP-dependent molecular chaperone, and over-expressed in a variety of tumor cells. Some molecules that play important roles in tumor development signaling pathways such as epidermal growth factor receptor (EGFR), human epidermal growth factor receptor-2 (HER2) are Hsp90AB1 client proteins. Hsp90AB1 interact with these client proteins and participate in a variety of pathophysiological processes of cells. The aim of this study is to detect the expression of Hsp90AB1 in non-small cell lung cancer (NSCLC) tissues, and explore its clinical significance. Methods The expression of Hsp90AB1 in 213 NSCLC tissues and 147 normal lung tissues was detected by tissue microarray and immunohistochemical staining method, and the relationship of Hsp90AB1 expression with clinicopathological parameters and prognosis of NSCLC patients were analyzed. Results The expression level of Hsp90AB1 in lung cancer tissues (positive rate of 54.0%) was significantly higher than that in normal lung tissue (positive rate of 0.0%, P0.05). Conclusion Hsp90AB1 protein was over-expressed in NSCLC tissues, and was associated with lung cancer pathological type and overall survival in lung adenocarcinoma patients.

Background and objective It has been proven that epithelial-mesenchymal transition (EMT) is a critical process which is precisely regulated by multiple signaling pathways during the progression and metastasis of non-small cell lung cancer (NSCLC). Canonical MAPK signaling is essential to transforming growth factor β (TGFβ)-induced EMT. Using the NSCLC cell line A549 as a model, the aim of this study is to explore the molecular mechanism of ENO1 affecting EMT. Methods We established an A549 strain stably overexpressing ENO1. Cell mobility was measured by the wound-healing assay. EMT-related molecular alterations were detected by Western blot analysis. The effect of ENO1 on EMT was also detected by TGFβ-1-inducing assay. EGF-stimulating assay was performed to illustrate ERK1/2 phosphorylation changes resulting from ENO1 overexpression. Results Overexpressed ENO1 inhibited the mobility of A549 (P

Background and objective Proper tumor markers are useful to diagnosis, prognosis and treatment for lung cancer. The aim of this study is to examine the levels of alpha-enolase (ENO1) protein in the tumor tissues and peripheral plasma samples obtained from non-small cell lung cancer (NSCLC) patients, and evaluate its potential clinical significance. Methods The ENO1 protein levels in the tumor tissues and corresponding normal tissues from 16 cases of lung squamous cell carcinoma were analyzed by Western blot. The ENO1 protein levels in the plasma samples from 42 healthy individuals, 34 patients with lung benign disease and 84 patients with NSCLC were measured by double antibody sandwich enzyme-linked immunosorbent assay. Results For 87.5% (14/16) of the patients with lung squamous cell carcinoma, the ENO1 protein level in the tumor tissues was higher than that in the corresponding normal lung tissues. The ENO1 protein level in the plasma of NSCLC patients was significantly higher than that in the plasma of healthy individuals (P=0.031) and patients with lung benign disease (P=0.019). Furthermore, the ENO1 protein level was significantly higher in the plasma of patients with lung adenocarcinoma than that of patients with lung squamous cell carcinoma. Conclusion The elevated levels of ENO1 protein in the tumor tissues and the plasma samples from NSCLC patients indicate ENO1 may be a candidate biomarker of lung cancer.

Background and objective The imprinted gene dlk1 has been recognized as a cancer related gene since it aberrantly expressed in a series of cancer tissues, but its role in lung cancer is still unknown. The aim of this study is to examine dlk1’s expression in non-small cell lung cancers (NSCLCs) and investigate the molecular mechanism by which dlk1 could accelerate the proliferation of the cells in lung cancer cell lines (H520). Methods The relative expression of dlk1 among 30 NSCLC specimens and their adjacent normal lung tissues were analyzed by RT-PCR. A cell model that stably expressed exogenous dlk1 was established following that the dlk1 gene was cloned into a eukaryotic expression vector and then transfected into the lung cancer cells H520. CCK8 analysis and colony forming assay were employed to investigate the effect of dlk1 on cell proliferation. The expression of CyclinB1 was detected by Western blot. Results dlk1 aberrantly expressed in 36.7% (11/30) of the tumor tissues of NSCLC compared with their adjacent cancer lung tissues. CCK8 analysis showed that overexpression of dlk1 could promote the proliferation of H520 cells (P < 0.05) and the results was further confirmed by colony forming assay. Western blot analysis found that over expression of dlk1 could up-regulate the expression of CyclinB1 (P < 0.05). Conclusion dlk1 aberrantly expressed in NSCLCs. The Overexpression of dlk1 could accelerate the proliferation of lung cancer cells H520 in vitro, probably through up-regulating the expression of cell cycle protein CyclinB1.