38 research outputs found

    PI3K/AKT/mTOR signaling in gastric cancer : epigenetics and beyond.

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    PI3K/AKT/mTOR pathway is one of the most important signaling pathways involved in normal cellular processes. Its aberrant activation modulates autophagy, epithelial-mesenchymal transition, apoptosis, chemoresistance, and metastasis in many human cancers. Emerging evidence demonstrates that some infections as well as epigenetic regulatory mechanisms can control PI3K/AKT/mTOR signaling pathway. In this review, we focused on the role of this pathway in gastric cancer development, prognosis, and metastasis, with an emphasis on epigenetic alterations including DNA methylation, histone modifications, and post-transcriptional modulations through non-coding RNAs fluctuations as well as H. pylori and Epstein-Barr virus infections. Finally, we reviewed different molecular targets and therapeutic agents in clinical trials as a potential strategy for gastric cancer treatment through the PI3K/AKT/mTOR pathway. [Abstract copyright: Copyright © 2020 Elsevier Inc. All rights reserved.

    Augmented expression levels of lncRNAs ecCEBPA and UCA1 in gastric cancer tissues and their clinical significance

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    Objective(s): As the second cause of cancer death, gastric cancer (GC) is one of the eminent dilemmas all over the world, therefore investigating the molecular mechanisms involved in this cancer is pivotal. Unrestricted proliferation is one of the characteristics of cancerous cells, which is due to deficiency in cell regulatory systems. Long non-coding RNAs (lncRNAs) have emerged as critical regulators of the epigenome. lncRNA extra coding CEBPA (ecCEBPA) is involved in DNA methylation. This lncRNA reduces CEBPA promoter methylation by interacting with DNA methyltransferase 1. lncRNA UCA1 (urothelial carcinoma-associated 1) elevates cell proliferation through the PI3K/Akt signaling pathway which has a critical role in cell growth and apoptosis. The aim of this study was to examine the expression of ecCEBPA and UCA1 genes in GC tissues as well as their clinical significance. Materials and Methods: Total RNA extraction, cDNA synthesis, and quantitative real-time PCR were performed for cells and 80 paired GC tissues. Furthermore, clinical relevance of UCA1 expression was investigated in TCGA cohort data. Results: Our results showed ecCEBPA and UCA1 over-expression in GC tissues. Furthermore, lncRNAs associations with clinicopathological features were demonstrated both in the current and TCGA cohort. Kaplan-Meier analysis indicated that patients with higher UCA1 expression had a worse overall survival in the case of pancreatic and lung adenocarcinomas but not other solid cancer types including GC. Conclusion: These data demonstrate UCA1 and ecCEBPA involvement in GC and suggest that these lncRNAs might be useful as diagnostic/ prognostic biomarkers in cancer

    A novel aerodynamic controllable roof for improving performance of INVELOX wind delivery system

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    INVELOX is a patented structure designed to capture the incident wind from every direction, guide the collected wind to the ground level, and increase its velocity. A novel mechanism called aerodynamic controllable roof structure is introduced to improve the wind stream performance of INVELOX. The advantages of aerodynamic controllable roof structure are twofold: improving efficiency and preventing wind escaping the system. Using aerodynamic controllable roof structure, a performance curve is obtained that can improve the system efficiency. Wind speed and orientation and structural deflection are the parameters that direct the roof orientation. Fuzzy control is utilized in a model structure to control the roof movements using two servo motors. Computational fluid dynamics simulations are done to validate the performance and capability of the aerodynamic controllable roof structure mechanism. Results show that the fuzzy control is successful in controlling the roof orientation and the results from the simulation indicate that the efficiency of the system can be increased up to 12%. </jats:p
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