BackgroundPropofol is one of the most commonly used intravenous anaesthetic agents during cancer resection surgery, but the effect of propofol on gallbladder cancer is not clear. NF-E2-related factor 2 (Nrf2) is abundantly expressed in cancer cells and relates to proliferation, invasion, and chemoresistance. The aims of the current study were to evaluate effects of propofol on the behavior of human GC cells and role of Nrf2 in these effects.MethodThe effects of propofol on cell proliferation, apoptosis, and invasion were detected by MTT assays, flow cytometry, and transwell assay. Also, activation of Nrf2 was determined by western blot, RT-PCR, and immunofluorescence assays. Nrf2 was knocked-down in GBC-SD cells by shRNA before evaluating the role of Nrf2 in the influence of propofol on biological behaviors.ResultsPropofol promoted the proliferation of GBC-SD cells in a dose- and time- dependent manner. After exposure to propofol for 48 h, GBC-SD cells showed decreased apoptosis and increased invasion. Also, propofol over-expressed Nrf2 at both the protein and mRNA levels and induced translocation of Nrf2 into the nucleus. Finally, loss of Nrf2 by shRNA reversed the effect of propofol on cell proliferation, apoptosis, and invasion.ConclusionPropofol induces proliferation and promotes invasion of GC cells through activation of Nrf2.

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Three-dimensional (3D) printing continuous carbon fiber-reinforced polylactic acid (PLA) composites offer excellent tensile mechanical properties. The present study aimed to research the effect of process parameters on the tensile mechanical properties of 3D printing composite specimens through a series of mechanical experiments. The main printing parameters, including layer height, extrusion width, printing temperature, and printing speed are changed to manufacture specimens based on the modified fused filament fabrication 3D printer, and the tensile mechanical properties of 3D printing continuous carbon fiber-reinforced PLA composites are presented. By comparing the outcomes of experiments, the results show that relative fiber content has a significant impact on mechanical properties and the ratio of carbon fibers in composites is influenced by layer height and extrusion width. The tensile mechanical properties of continuous carbon fiber-reinforced composites gradually decrease with an increase of layer height and extrusion width. In addition, printing temperature and speed also affect the fiber matrix interface, i.e., tensile mechanical properties increase as the printing temperature rises, while the tensile mechanical properties decrease when the printing speed increases. Furthermore, the strengthening mechanism on the tensile mechanical properties is that external loads subjected to the components can be transferred to the carbon fibers through the fiber-matrix interface. Additionally, SEM images suggest that the main weakness of continuous carbon fiber-reinforced 3D printing composites exists in the fiber-matrix interface, and the main failure is the pull-out of the fiber caused by the interface destruction.

BackgroundErbB4 expression has been noted in various tumors, but its regulatory mechanism in esophageal squamous cell carcinoma (ESCC) remains unclear. The aim of this study was to investigate whether miR-302b regulates the expression of ErbB4 at the post-transcriptional level and to determine its expression, significance, and function in ESCC.MethodsWe used real-time reverse transcriptase-polymerase chain reaction to quantify the expression of miR-302b in 50 ESCC tissues and analyzed its relationship with clinicopathological factors and survival. Then, we investigated the post-transcriptional regulation of ErbB4 expression using immunoblot analysis and luciferase reporter assays. Finally, the effects of miR-302b on proliferation, apoptosis, and invasion of ESCC cells was detected using MTT, flow cytometric analysis, and transwell invasion assays, respectively.ResultsmiR-302b was significantly down-regulated and correlated with tumor differentiation and lymph node metastasis in ESCC. Univariate and multivariate analyses indicated that low miR-302b expression might be a poor prognostic factor. Further studies demonstrated that miR-302b post-transcriptionally down-regulated the expression of ErbB4 in vitro. Moreover, miR-302b inhibited proliferation by inducing apoptosis and repressed invasion in the ESCC cell lines.ConclusionsmiR-302b is a potential molecular marker of ESCC and functions as a tumor suppressor by post-transcriptionally regulating ErbB4.

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BackgroundX-chromosome-linked IAP (XIAP) and nuclear factor-κB (NF-κB) are frequently overexpressed and correlate closely with chemoradiotherapy resistance and poor prognosis in many cancers. However, the significance of XIAP and NF-κB expression in radiotherapy sensitivity and its effect on the prognosis of esophageal squamous cell carcinoma (ESCC) are still unknown. The aim of this study was to examine XIAP and NF-κB status in ESCC patients undergoing postoperative radiotherapy after radical surgery, and to evaluate their clinical significance.MethodsA total of 78 ESCC patients treated with postoperative radiotherapy after radical surgery were enrolled in this study. We immunohistochemically investigated the expression of XIAP and NF-κB in tissues from enrolled patients with specific antibodies. Then, the correlations among XIAP, NF-κB expression, clinicopathological features and its prognostic relevance in ESCC were analyzed.ResultsThe increased expression of XIAP and NF-κB in ESCC tissues were clearly correlated with the tumor differentiation and p-TNM stage. Significant positive correlations were found between the expression status of XIAP and NF-κB (r = 0.779, P = 0.000). Overexpression of XIAP and NF-κB and metastasis were significantly associated with shorter overall survival times in univariate analysis (P < 0.05). Multivariate analysis also confirmed that XIAP expression was an independent prognostic factor (P = 0.005).ConclusionsXIAP and NF-κB are intensively expressed in ESCC. The level of XIAP is positively correlated to progression and prognosis of ESCC.

Cancer related inflammation (CRI) plays an important role in the development of esophageal cancer (EC), and the target gene analysis shows that miR-302b potential target genes closely correlated to CRI important signaling pathways. The present study was to evaluate the inhibition of miR-302b on CRI in EC and its mechanism. We found that the expression levels of miR-302b in EC cells were lower than that in Het-1A cells, while TE11 with the lowest expression and OE33 with the highest. Inflammatory stimuli at 48 h significantly reduced expression of miR-302b in EC cells, but had no effect in Het-1A. After up-regulation of miR-302b in TE11 and down-regulation of miR-302b in OE33, it was found that miR-302b reduced CRI key transcription factors and representative cytokines. Then, over-expressed of miR-302b significantly altered potential target genes protein expressions and there was a negative correlation between miR-302b and potential target genes protein expressions (ERBB4, IRF2 and CXCR4) in EC tissues. Then reporter gene analysis revealed that miR-302b post-transcriptionally regulated expression of target genes by specific area of 3′-UTR. Transfected by target genes shRNA plasmids together could get the same effects of miR-302b on protein expression of CRI key transcription factors. Furthermore, miR-302b was able to repress tumor growth and transcription factors protein expression in vivo. These finding suggests that miR-302b inhibits key transcription factors and cytokines by targeting ERBB4, IRF2 and CXCR4, implicating its role in the inhibition of CRI in EC.

To date, preclinical and clinical data have shown that various cancer patients benefit from antiangiogenic therapy because of the important role of angiogenesis in the tumor development process. NF-E2-related factor 2 (Nrf2) is recognized as a key transcription factor of genes coding for various antioxidant and cytoprotective enzymes, and Nrf2 plays important roles during tumor progression. Recent studies have begun to explore the role of Nrf2 in tumor angiogenesis, which may be to promote the advancement of tumor antiangiogenic therapy. This article reviews the Nrf2-related pathways involved in tumor angiogenesis and summarizes the possible mechanisms of Nrf2 action as a pro-angiogenic factor in tumor progression.