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Special Issue "Marine Compounds as Modulators of Autophagy and Lysosomal Activity"

A special issue of Marine Drugs (ISSN 1660-3397).

Deadline for manuscript submissions: 31 December 2017

Special Issue Editors

Guest Editor
Dr. Friedemann Honecker

Tumor and Breast Center ZeTuP St. Gallen, Rorschacherstr. 150, CH-9006 St. Gallen, Switzerland
Website | E-Mail
Fax: +41 71 2430 044
Interests: medical oncology; drug resistance; marine anti-cancer compounds; drug development; tumor biology; proteomics
Guest Editor
Dr. Sergey A. Dyshlovoy

1 Laboratory of Marine Natural Products Chemistry, G.B. Elyakov Pacific Institute of Bioorganic Chemistry FEB RAS, Prospekt 100-let Vladivostoku 159 (room 312), 690022 Vladivostok, Russia
2 Laboratory of Experimental Oncology, Department of Internal Medicine II and Clinic (Oncology Center), University Medical Center Hamburg-Eppendorf, Martinistr. 52 (N27, room 4.082), 20246 Hamburg, Germany
E-Mail
Phone: +49 40 7410 55896
Fax: +7 423 2314050
Interests: bioactive marine natural products; autophagy; molecular mechanism of anticancer activity; drug target identification and validation; proteomics; drug combination studies.

Special Issue Information

Dear Colleagues,

In 2016, the Nobel Prize in Physiology or Medicine has been awarded to Prof. Yoshinori Ohsumi for the discoveries of mechanisms of autophagy. Autophagy is a basic physiological process, which has only recently received a lot of attention. This cellular process, which is implicated in many aspects of human physiology and disease, including tissue homeostasis, cancer, neurodegenerative conditions (Parkinson's and Alzheimer's disease), cardiomyopathy, and others, is essential for the survival and death of mammalian cells. Thus, it is an exciting perspective to find and develop compounds that have the ability to control and modify this process.
Lysosomes are an essential part of the autophagy machinery which plays a role at the final stages of this process, providing the degradation of the autophagosomes content. Furthermore, lysosomes participate in a vast number of physiological and pathological processes, and may play a role in both drug sensitivity and drug resistance. Several clinically approved compounds target lysosomes as their mode of action.
Compared to terrestrial life forms, marine inhabitants are by far less well studied organisms. At the same time, due to the extreme environmental conditions (high pressure, lack of light, salinity, pH), they harbor a unique variety of chemical compounds, of which a large number still await discovery and characterization. A good proportion of these compounds exhibit potent biological activity, targeting one or several specific biological processes.
This Special Issue “Marine Compounds as Modulators of Autophagy and Lysosomal Activity” in Marine Drugs will cover the whole scope of agents targeting autophagy or/and lysosomes both in vitro and in vivo – novel to previously characterized, including already clinically used marine derived compounds. This Special issue is focused on (but not limited to!) compounds that affect autophagy and lysosomes in malignant cells. In particular, the issue will collect work on compounds that are able to target lysosomes and modulate all the different types of autophagy – i.e. macroautophagy, microautophagy, and chaperone-mediated autophagy – with cytotoxic, cytoprotective, pro-survival, or non-cytotoxic biological activity.
Since autophagy is a relatively new and sometimes still controversial topic, results of similar experiments are often interpreted in different ways. Therefore, the Guest Editors suggest to use the recommendations recently described by Klionsky et al. in the “Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)” (Autophagy. 2016;12(1):1-222; PMID: 26799652) for interpretation of experimental data submitted to this Special Issue.

Sergey A. Dyshlovoy
Friedemann Honecker,
Guest Editors

Keywords

• autophagy
• macroautophagy
• lysosomes
• lysosomal membrane permeabilization (LMP)
• cathepsins
• marine compounds
• cell death
• cell survival
• drug resistance
• necrosis
• cancer
• neurodegenerative disease

Published Papers (3 papers)

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Research

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Open AccessArticle Quantitative Proteomic Profiling of Tachyplesin I Targets in U251 Gliomaspheres
Mar. Drugs 2017, 15(1), 20; doi:10.3390/md15010020
Received: 20 November 2016 / Revised: 5 January 2017 / Accepted: 12 January 2017 / Published: 18 January 2017
PDF Full-text (3978 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Tachyplesin I is a cationic peptide isolated from hemocytes of the horseshoe crab and its anti-tumor activity has been demonstrated in several tumor cells. However, there is limited information providing the global effects and mechanisms of tachyplesin I on glioblastoma multiforme (GBM). Here,
[...] Read more.
Tachyplesin I is a cationic peptide isolated from hemocytes of the horseshoe crab and its anti-tumor activity has been demonstrated in several tumor cells. However, there is limited information providing the global effects and mechanisms of tachyplesin I on glioblastoma multiforme (GBM). Here, by using two complementary proteomic strategies (2D-DIGE and dimethyl isotope labeling-based shotgun proteomics), we explored the effect of tachyplesin I on the proteome of gliomaspheres, a three-dimensional growth model formed by a GBM cell line U251. In total, the expression levels of 192 proteins were found to be significantly altered by tachyplesin I treatment. Gene ontology (GO) analysis revealed that many of them were cytoskeleton proteins and lysosomal acid hydrolases, and the mostly altered biological process was related to cellular metabolism, especially glycolysis. Moreover, we built protein–protein interaction network of these proteins and suggested the important role of DNA topoisomerase 2-alpha (TOP2A) in the signal-transduction cascade of tachyplesin I. In conclusion, we propose that tachyplesin I might down-regulate cathepsins in lysosomes and up-regulate TOP2A to inhibit migration and promote apoptosis in glioma, thus contribute to its anti-tumor function. Our results suggest tachyplesin I is a potential candidate for treatment of glioma. Full article
(This article belongs to the Special Issue Marine Compounds as Modulators of Autophagy and Lysosomal Activity)
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Figure 1

Open AccessArticle Tumor Protein (TP)-p53 Members as Regulators of Autophagy in Tumor Cells upon Marine Drug Exposure
Mar. Drugs 2016, 14(8), 154; doi:10.3390/md14080154
Received: 2 June 2016 / Revised: 17 July 2016 / Accepted: 9 August 2016 / Published: 16 August 2016
Cited by 2 | PDF Full-text (1912 KB) | HTML Full-text | XML Full-text | Supplementary Files
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
[...] Read more.
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. Full article
(This article belongs to the Special Issue Marine Compounds as Modulators of Autophagy and Lysosomal Activity)
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Review

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Open AccessReview Blue-Print Autophagy: Potential for Cancer Treatment
Mar. Drugs 2016, 14(7), 138; doi:10.3390/md14070138
Received: 22 June 2016 / Revised: 11 July 2016 / Accepted: 14 July 2016 / Published: 21 July 2016
Cited by 2 | PDF Full-text (1353 KB) | HTML Full-text | XML Full-text
Abstract
The marine environment represents a very rich source of biologically active compounds with pharmacological applications. This is due to its chemical richness, which is claiming considerable attention from the health science communities. In this review we give a general overview on the marine
[...] Read more.
The marine environment represents a very rich source of biologically active compounds with pharmacological applications. This is due to its chemical richness, which is claiming considerable attention from the health science communities. In this review we give a general overview on the marine natural products involved in stimulation and inhibition of autophagy (a type of programmed cell death) linked to pharmacological and pathological conditions. Autophagy represents a complex multistep cellular process, wherein a double membrane vesicle (the autophagosome) captures organelles and proteins and delivers them to the lysosome. This natural and destructive mechanism allows the cells to degrade and recycle its cellular components, such as amino acids, monosaccharides, and lipids. Autophagy is an important mechanism used by cells to clear pathogenic organism and deal with stresses. Therefore, it has also been implicated in several diseases, predominantly in cancer. In fact, pharmacological stimulation or inhibition of autophagy have been proposed as approaches to develop new therapeutic treatments of cancers. In conclusion, this blue-print autophagy (so defined because it is induced and/or inhibited by marine natural products) represents a new strategy for the future of biomedicine and of biotechnology in cancer treatment. Full article
(This article belongs to the Special Issue Marine Compounds as Modulators of Autophagy and Lysosomal Activity)
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Marine Drugs Editorial Office
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