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oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/147502026-10-18T21:14:24Zopenairedrivercom_ebyu_10000col_ebyu_10001

Synthesis and bio-molecular study of (+)-N-Acetyl-α-amino acid dehydroabietylamine derivative for the selective therapy of hepatocellular carcinomaMustufa, Muhammad AyazOzen, CigdemHashmi, Imran AliAslam, AfshanBaig, Jameel AhmedYildiz, GokhanMuhammad, ShoaibSolangi, Imam Bakhshul Hasan Naqvi, NaimOzturk, MehmetAli, Firdous ImranApoptosisConnectivity mapCytotoxicityDehydroabietylamine derivativesHepatocellular carcinomaAntineoplastic AgentsCarcinoma, HepatocellularCaspasesCell CycleCell Line, TumorCell ProliferationDiterpenes, AbietaneG2 Phase Cell Cycle CheckpointsHumansInhibitory Concentration 50Liver Neoplasmscamptothecincaspasecytotoxic agentn (n acetyl cysteine)dehydroabietylamineunclassified drugabietane derivativeantineoplastic agentdehydroabietylamineArticleattenuationcell structurecontrolled studydrug cytotoxicitydrug effectBackground: The purpose of present work is to synthesize novel (+)-Dehydroabietylamine derivatives (DAAD) using N-acetyl-α-amino acid conjugates and determine its cytotoxic effects on hepatocellular carcinoma cells. Methods: An analytical study was conducted to explore cytotoxic activity of DAAD on hepatocellular carcinoma cell lines. The cytotoxicity effect was recorded using sulforhodamine B technique. Cell cycle analysis was performed using Propidium Iodide (PI) staining. Based on cell morphology, anti growth activity and microarray findings of DAAD2 treatment, Comet assay, Annexin V/PI staining, Immunoperoxidase assay and western blots were performed accoringly. Results: Hep3B cells were found to be the most sensitive with IC50 of 2.00 ± 0.4 μM against (+)-N-(N-Acetyl-L-Cysteine)-dehydroabietylamine as DAAD2. In compliance to time dependent morphological changes of low cellular confluence, detachment and rounding of DAAD2 treated cells; noticeable changes in G2/M phase were recorded may be leading to cell cycle cessation. Up-regulation (5folds) of TUBA1A gene in Hep3B cells was determined in microarray experiments. Apoptotic mode of cell death was evaluated using standardized staining procedures including comet assay and annexin V/PI staining, Immuno-peroxidase assay. Using western blotting technique, caspase dependant apoptotic mode of cell death was recorded against Hep3B cell line. Conclusion: It is concluded that a novel DAAD2 with IC50 values less than 8 μM can induce massive cell attenuation following caspase dependent apoptotic cell death in Hep3B cells. Moreover, the corelation study indicated that DAAD2 may have vital influence on cell prolifration properties. © 2016 The Author(s).BioMed Central Ltd.2016Articlehttps://rdlopen.rawdatalibrary.net/r/ebyu/14750https://doi.org/10.1186/s12885-016-2942-51471-2407enBMC Cancerinfo:eu-repo/semantics/openAccessinfo:eu-repo/semantics/articlehttps://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/14750