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Mar. Drugs 2016, 14(8), 154; doi:10.3390/md14080154

Tumor Protein (TP)-p53 Members as Regulators of Autophagy in Tumor Cells upon Marine Drug Exposure

Head and Neck Cancer Research Division, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
Academic Editors: Friedemann Honecker and Sergey A. Dyshlovoy
Received: 2 June 2016 / Revised: 17 July 2016 / Accepted: 9 August 2016 / Published: 16 August 2016
(This article belongs to the Special Issue Marine Compounds as Modulators of Autophagy and Lysosomal Activity)
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Abstract

Targeting autophagic pathways might play a critical role in designing novel chemotherapeutic approaches in the treatment of human cancers, and the prevention of tumor-derived chemoresistance. Marine compounds were found to decrease tumor cell growth in vitro and in vivo. Some of them were shown to induce autophagic flux in tumor cells. In this study, we observed that the selected marine life-derived compounds (Chromomycin A2, Psammaplin A, and Ilimaquinone) induce expression of several autophagic signaling intermediates in human squamous cell carcinoma, glioblastoma, and colorectal carcinoma cells in vitro through a transcriptional regulation by tumor protein (TP)-p53 family members. These conclusions were supported by specific qPCR expression analysis, luciferase reporter promoter assay, and chromatin immunoprecipitation of promoter sequences bound to the TP53 family proteins, and silencing of the TP53 members in tumor cells. View Full-Text
Keywords: marine drugs; cancer; autophagy; p53 family members; transcription marine drugs; cancer; autophagy; p53 family members; transcription
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Ratovitski, E.A. Tumor Protein (TP)-p53 Members as Regulators of Autophagy in Tumor Cells upon Marine Drug Exposure. Mar. Drugs 2016, 14, 154.

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