Heat shock protein 27 is over-expressed in tumor tissues and increased in sera of patients with gastric adenocarcinoma

Background: In a previous study, we found that heat shock protein 27 (HSP27) was over-expressed in gastric adenocarcinoma (GA) tissue. In this study, our goal was to further verify the expression profile of HSP27 in patients with GA. Methods: Western blot and immunohistochemistry were employed to determine HSP27 expression in 50 paired tumor and adjacent normal tissue. ELISA was used to quantify serum HSP27 concentrations in the same 50 GA patients and 50 healthy individuals. Results: Compared to adjacent normal tissues, HSP27 was over-expressed in 25 (50%, p=0.000) and 24 (48%, p=0.000) cases of GA tissue by Western blot and immunohistochemistry, respectively. ELISA revealed significantly higher serum concentrations of HSP27 in patients with GA patients (mean=986 pg/mL) compared to healthy individuals (mean=573 pg/mL) (p=0.003). In addition, infection with Helicobacter pylori (HP) in healthy individuals was associated with increased expression of HSP27 in both gastric mucosa and serum. Conclusions: These data suggest that HSP27 is over-expressed in GA tissue and serum concentrations of HSP27 are increased in patients with GA. Over-expression of HSP27 may indicate a gastric malignant/infectious process. The detection of serum HSP27 concentrations by ELISA may be useful for screening for GA. Clin Chem Lab Med 2010;48:263–9.Peer Reviewe

Kindlin-2 promotes hepatocellular carcinoma invasion and metastasis by increasing Wnt/β-catenin signaling

Abstract Background Kindlin-2 is a member of the focal adhesion protein family that regulates invasion and metastasis in multiple malignancies; however, little is known about the role of Kindlin-2 in hepatocellular carcinoma (HCC) progression. Methods Immunohistochemistry was used to investigate Kindlin-2 expression in 177 pairs of human HCC and adjacent liver tissue samples. The role of Kindlin-2 in the in vitro invasion and migration of HCC cell lines was evaluated in MHCC97H, LM3 and SMMC7721 cells. Microarray expression analysis was applied to explore the molecular mechanism through which Kindlin-2 promoted HCC progression. Quantitative real-time PCR and Western blotting were performed to verify the microarray results. Results High Kindlin-2 expression was found to significantly correlate with aggressive HCC clinicopathological features including tumor encapsulation, microvascular invasion, extrahepatic metastasis and poor prognosis. In vitro, Kindlin-2 knockout or knockdown inhibited HCC cell adhesion, migration and invasion, while ectopic Kindlin-2 expression promoted these processes. Importantly, Kindlin-2 activated Wnt/β-catenin signaling and increased β-catenin expression, especially levels of non-phosphorylated β-catenin, as well as two Wnt/β-catenin signaling pathway targets, Axin2 and MMP7. Kindlin-2 also induced a change in the expression profile of HCC cells, suggesting the cells underwent epithelial-mesenchymal transition. For example, the expression of the epithelial marker E-cadherin was downregulated, while the mesenchymal markers Vimentin, N-cadherin and Snail were upregulated. Conclusion Kindlin-2 promotes HCC invasion, metastasis and epithelial-mesenchymal transition through Wnt/β-catenin signaling

Correction to: EBV-miR-BART8-3p induces epithelial-mesenchymal transition and promotes metastasis of nasopharyngeal carcinoma cells through activating NF-κB and Erk1/2 pathways

Following publication of the original article [1], the authors reported two errors in the article. In the caption of Figure 1c the sentence “The 20 most highly upregulated EBV BART miRNAs identified between NPC specimens and normal nasopharyngeal mucosal specimens" should be corrected as “The highly upregulated EBV BART miRNAs identified between NPC specimens and normal nasopharyngeal mucosal specimens”

Effect of Bromine Substitution on the Ion Migration and Optical Absorption in MAPbI₃ Perovskite Solar Cells: The First-Principles Study

In the past few years, the remarkable energy conversion efficiency of lead-halide-based perovskite solar cells (PSCs) has drawn extraordinary attention. However, some exposed problems in PSCs such as the low chemical stability and so forth are tough to eliminate. A fundamental understanding of ionic transport at the nanoscale is essential for developing high-performance PSCs based on the anomalous hysteresis current–voltage (<i>I</i>–<i>V</i>) curves and the poor stability. Our work is to understand the ionic transport mechanism by introducing suitable halogen substitution with insignificant impact on light absorption to hinder ion diffusion and thereby to seek a method to improve the stability. Herein, we used first-principles density functional theory (DFT) to calculate the band gaps and the optical absorption coefficients, and the interstitial and the vacancy defect diffusion barriers of halide in the orthogonal phase MAPbX₃ (MA = CH₃NH₃, X = I, Br, I_0.5Br_0.5) perovskite, respectively. The research results show that a half bromine substitution not only prevents ion migration in perovskite, but also maintains a favorable light absorption capacity. It may be helpful to maintain the PSC’s property of light absorption with a similar atomic substitution. Furthermore, smaller atomic substitution for the halogen atoms may be essential for increasing the diffusion barrier