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Lipidated lc3, lung cancer

Jonathan Mandelbaum, Neil Rollins, Pooja Shah, Doug Bowman, Janice Y Lee, Olga Tayber, Hugues Bernard, Patrick LeRoy, Ping Li, Erik Koenig, James E Brownell, Natalie D'Amore
Autophagy is a major cellular process for bulk degradation of proteins and organelles in order to maintain metabolic homeostasis, and it represents an emerging target area for cancer. Initially proposed to be a cancer-restricting process for tumor initiation, recent studies suggest that autophagy can also promote cell survival in established tumors. ATG7 is an essential autophagy gene that encodes the E1 enzyme necessary for the lipidation of the LC3 family of ubiquitin-like proteins and autophagosome formation...
June 19, 2015: Autophagy
Ming-Ju Hsieh, Te-Lung Tsai, Yih-Shou Hsieh, Chau-Jong Wang, Hui-Ling Chiou
Our previous study has revealed that dioscin, a compound with anti-inflammatory, lipid-lowering, anticancer and hepatoprotective effects, may induce autophagy in hepatoma cells. Autophagy is a lysosomal degradation pathway that is essential for cell survival and tissue homeostasis. In this study, the role of autophagy and related signaling pathways during dioscin-induced apoptosis in human lung cancer cells was investigated. Results from 4'-6-diamidino-2-phenylindole and annexin-V/PI double-staining assay showed that caspase-3- and caspase-8-dependent, and dose-dependent apoptoses were detected after a 24-h dioscin treatment...
November 2013: Archives of Toxicology
Vitaliy O Kaminskyy, Tatiana Piskunova, Irina B Zborovskaya, Elena M Tchevkina, Boris Zhivotovsky
Autophagy is a catabolic process involved in the turnover of organelles and macromolecules which, depending on conditions, may lead to cell death or preserve cell survival. We found that some lung cancer cell lines and tumor samples are characterized by increased levels of lipidated LC3. Inhibition of autophagy sensitized non-small cell lung carcinoma (NSCLC) cells to cisplatin-induced apoptosis; however, such response was attenuated in cells treated with etoposide. Inhibition of autophagy stimulated ROS formation and treatment with cisplatin had a synergistic effect on ROS accumulation...
July 1, 2012: Autophagy
Giampietro Viola, Roberta Bortolozzi, Ernest Hamel, Stefano Moro, Paola Brun, Ignazio Castagliuolo, Maria Grazia Ferlin, Giuseppe Basso
We previously demonstrated that MG-2477 (3-cyclopropylmethyl-7-phenyl-3H-pyrrolo[3,2-f]quinolin-9(6H)-one) inhibits the growth of several cancer cell lines in vitro. Here we show that MG-2477 inhibited tubulin polymerization and caused cells to arrest in metaphase. The detailed mechanism of action of MG-2477 was investigated in a non-small cell lung carcinoma cell line (A549). Treatment of A549 cells with MG-2477 caused the cells to arrest in the G2/M phase of the cell cycle, with a concomitant accumulation of cyclin B...
January 1, 2012: Biochemical Pharmacology
Saeid Ghavami, Mark M Mutawe, Pawan Sharma, Behzad Yeganeh, Karol D McNeill, Thomas Klonisch, Helmut Unruh, Hessam H Kashani, Dedmer Schaafsma, Marek Los, Andrew J Halayko
Statins inhibit the proximal steps of cholesterol biosynthesis, and are linked to health benefits in various conditions, including cancer and lung disease. We have previously investigated apoptotic pathways triggered by statins in airway mesenchymal cells, and identified reduced prenylation of small GTPases as a primary effector mechanism leading to p53-mediated cell death. Here, we extend our studies of statin-induced cell death by assessing endpoints of both apoptosis and autophagy, and investigating their interplay and coincident regulation...
2011: PloS One
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