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Marine Drugs
Special Issues
Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents
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Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents

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

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 14927

Special Issue Editors

Prof. Dr. Jane E. Ishmael

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy, Oregon State University, 1601 SW Jefferson Avenue, Corvallis, OR, 97331, USA
Interests: cell signaling; protein secretion; ER stress; autophagy; cancer cell death; cytoskeleton; glioblastoma
Prof. Dr. Valery Dembitsky

E-Mail Website
Guest Editor
Centre for Applied Research, Innovation and Entrepreneurship, Lethbridge College, 3000 College Drive South, Lethbridge, AB T1K 1L6, Canada
Interests: actinobacteria; fungal endophytes; yeast; microscopic fungi; microalgae; cyanobacteria; lichens; alkaloids; terpenoids; aromatic; lipids; fatty acids; peptides; antitumor; antiviral
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Marine flora and fauna, including bacteria, cyanobacteria, fungi, microalgae, algae, sponges, coelenterates, mollusks, echinoderms, and tunicates (ascidians), are extremely important ocean resources, accounting for over 90% of ocean biomass. These marine organisms also represent a rich source of diverse natural products with the potential to reveal new mechanisms of cell signaling and inspire anticancer drug development. Through collaborative and interdisciplinary approaches, several chemical structures of marine origin have progressed from discovery and structure elucidation to validation and final approval for use as therapeutic agents. In this Special Issue, entitled “Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents”, we will provide researchers with a platform for publishing basic chemical, pharmacological, and biomedical research relevant to the study of primary tumors or metastatic disease. We welcome contributions from scientists around the world with an emphasis on preclinical evaluation of new and known compounds.

Prof. Dr. Jane E. Ishmael
Prof. Dr. Valery Dembitsky
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Marine Drugs is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • antitumor agent
  • secondary metabolite
  • marine natural products
  • pharmacology
  • preclinical
  • drug discovery
  • cell signaling
  • microbial

Published Papers (5 papers)

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Research

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17 pages, 3676 KiB  
Article
Matairesinol Induces Mitochondrial Dysfunction and Exerts Synergistic Anticancer Effects with 5-Fluorouracil in Pancreatic Cancer Cells
by Woonghee Lee, Gwonhwa Song and Hyocheol Bae
Mar. Drugs 2022, 20(8), 473; https://doi.org/10.3390/md20080473 - 25 Jul 2022
Cited by 8 | Viewed by 2274
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive types of cancer and exhibits a devastating 5-year survival rate. The most recent procedure for the treatment of PDAC is a combination of several conventional chemotherapeutic agents, termed FOLFIRINOX, that includes irinotecan, leucovorin, [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive types of cancer and exhibits a devastating 5-year survival rate. The most recent procedure for the treatment of PDAC is a combination of several conventional chemotherapeutic agents, termed FOLFIRINOX, that includes irinotecan, leucovorin, oxaliplatin, and 5-fluorouracil (5-FU). However, ongoing treatment using these agents is challenging due to their severe side effects and limitations on the range of patients available for PDAC. Therefore, safer and more innovative anticancer agents must be developed. The anticarcinoma activity of matairesinol that can be extracted from seagrass has been reported in various types of cancer, including prostate, breast, cervical, and pancreatic cancer. However, the molecular mechanism of effective anticancer activity of matairesinol against pancreatic cancer remains unclear. In the present study, we confirmed the inhibition of cell proliferation and progression induced by matairesinol in representative human pancreatic cancer cell lines (MIA PaCa-2 and PANC-1). Additionally, matairesinol triggers apoptosis and causes mitochondrial impairment as evidenced by the depolarization of the mitochondrial membrane, disruption of calcium, and suppression of cell migration and related intracellular signaling pathways. Finally, matairesinol exerts a synergistic effect with 5-FU, a standard anticancer agent for PDAC. These results demonstrate the therapeutic potential of matairesinol in the treatment of PDAC. Full article
(This article belongs to the Special Issue Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents)
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20 pages, 2877 KiB  
Article
The Marine-Derived Macrolactone Mandelalide A Is an Indirect Activator of AMPK
by Daphne R. Mattos, Xuemei Wan, Jeffrey D. Serrill, Minh H. Nguyen, Ian R. Humphreys, Benoit Viollet, Amos B. Smith III, Kerry L. McPhail and Jane E. Ishmael
Mar. Drugs 2022, 20(7), 418; https://doi.org/10.3390/md20070418 - 27 Jun 2022
Cited by 4 | Viewed by 2828
Abstract
The mandelalides are complex macrolactone natural products with distinct macrocycle motifs and a bioactivity profile that is heavily influenced by compound glycosylation. Mandelalides A and B are direct inhibitors of mitochondrial ATP synthase (complex V) and therefore more toxic to mammalian cells with [...] Read more.
The mandelalides are complex macrolactone natural products with distinct macrocycle motifs and a bioactivity profile that is heavily influenced by compound glycosylation. Mandelalides A and B are direct inhibitors of mitochondrial ATP synthase (complex V) and therefore more toxic to mammalian cells with an oxidative metabolic phenotype. To provide further insight into the pharmacology of the mandelalides, we studied the AMP-activated protein kinase (AMPK) energy stress pathway and report that mandelalide A is an indirect activator of AMPK. Wild-type mouse embryonic fibroblasts (MEFs) and representative human non-small cell lung cancer (NSCLC) cells showed statistically significant increases in phospho-AMPK (Thr172) and phospho-ACC (Ser79) in response to mandelalide A. Mandelalide L, which also harbors an A-type macrocycle, induced similar increases in phospho-AMPK (Thr172) and phospho-ACC (Ser79) in U87-MG glioblastoma cells. In contrast, MEFs co-treated with an AMPK inhibitor (dorsomorphin), AMPKα-null MEFs, or NSCLC cells lacking liver kinase B1 (LKB1) lacked this activity. Mandelalide A was significantly more cytotoxic to AMPKα-null MEFs than wild-type cells, suggesting that AMPK activation serves as a protective response to mandelalide-induced depletion of cellular ATP. However, LKB1 status alone was not predictive of the antiproliferative effects of mandelalide A against NSCLC cells. When EGFR status was considered, erlotinib and mandelalide A showed strong cytotoxic synergy in combination against erlotinib-resistant 11-18 NSCLC cells but not against erlotinib-sensitive PC-9 cells. Finally, prolonged exposures rendered mandelalide A, a potent and efficacious cytotoxin, against a panel of human glioblastoma cell types regardless of the underlying metabolic phenotype of the cell. These results add biological relevance to the mandelalide series and provide the basis for their further pre-clinical evaluation as ATP synthase inhibitors and secondary activators of AMPK. Full article
(This article belongs to the Special Issue Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents)
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17 pages, 4175 KiB  
Article
(−)-Agelasidine A Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Human Hepatocellular Carcinoma
by I-Ta Lu, Shih-Chao Lin, Yi-Chia Chu, Ya Wen, You-Cheng Lin, Wen-Chien Cheng, Jyh-Horng Sheu and Chi-Chien Lin
Mar. Drugs 2022, 20(2), 109; https://doi.org/10.3390/md20020109 - 29 Jan 2022
Cited by 10 | Viewed by 3064
Abstract
Liver cancers, such as hepatocellular carcinoma (HCC), are a highly prevalent cause of cancer-related deaths. Current treatments to combat liver cancer are limited. (−)-Agelasidine A, a compound isolated from the methanol extract of Agelasnakamurai, a sesquiterpene guanidine derived from sea sponge, [...] Read more.
Liver cancers, such as hepatocellular carcinoma (HCC), are a highly prevalent cause of cancer-related deaths. Current treatments to combat liver cancer are limited. (−)-Agelasidine A, a compound isolated from the methanol extract of Agelasnakamurai, a sesquiterpene guanidine derived from sea sponge, has antibacterial activity. We demonstrated its anticancer capabilities by researching the associated mechanism of (−)-agelasidine A in human liver cancer cells. We found that (−)-agelasidine A significantly reduced viability in Hep3B and HepG2 cells, and we determined that apoptosis was involved in the (−)-agelasidine A-induced Hep3B cell deaths. (−)-Agelasidine A activated caspases 9, 8, and 3, as well as PARP. This effect was reversed by caspase inhibitors, suggesting caspase-mediated apoptosis in the (−)-agelasidine A-treated Hep3B cells. Moreover, the reduced mitochondrial membrane potential (MMP) and the release of cytochrome c indicated that the (−)-agelasidine A-mediated mitochondrial apoptosis was mechanistic. (−)-Agelasidine A also increased apoptosis-associated proteins (DR4, DR5, FAS), which are related to extrinsic pathways. These events were accompanied by an increase in Bim and Bax, proteins that promote apoptosis, and a decrease in the antiapoptotic protein, Bcl-2. Furthermore, our results presented that (−)-agelasidine A treatment bridged the intrinsic and extrinsic apoptotic pathways. Western blot analysis of Hep3B cells treated with (−)-agelasidine A showed that endoplasmic reticulum (ER) stress-related proteins (GRP78, phosphorylated PERK, phosphorylated eIF2α, ATF4, truncated ATF6, and CHOP) were upregulated. Moreover, 4-PBA, an ER stress inhibitor, could also abrogate (−)-agelasidine A-induced cell viability reduction, annexin V+ apoptosis, death receptor (DR4, DR5, FAS) expression, mitochondrial dysfunction, and cytochrome c release. In conclusion, by activating ER stress, (−)-agelasidine A induced the extrinsic and intrinsic apoptotic pathways of human HCC. Full article
(This article belongs to the Special Issue Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents)
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9 pages, 1355 KiB  
Article
Psammaceratin A: A Cytotoxic Psammaplysin Dimer Featuring an Unprecedented (2Z,3Z)-2,3-Bis(aminomethylene)succinamide Backbone from the Red Sea Sponge Pseudoceratina arabica
by Diaa T. A. Youssef, Hani Z. Asfour and Lamiaa A. Shaala
Mar. Drugs 2021, 19(8), 433; https://doi.org/10.3390/md19080433 - 29 Jul 2021
Cited by 8 | Viewed by 1691
Abstract
Bioassay-guided partition of the extract of the Red Sea sponge Pseudoceratina arabica and HPLC purification of the active fraction gave a psammaplysin dimer, psammaceratin A (1), along with psammaplysin A (2). The dimer comprises two units of psammaplysin A [...] Read more.
Bioassay-guided partition of the extract of the Red Sea sponge Pseudoceratina arabica and HPLC purification of the active fraction gave a psammaplysin dimer, psammaceratin A (1), along with psammaplysin A (2). The dimer comprises two units of psammaplysin A (2) connected via the terminal amines with an unprecedented (2Z,3Z)-2,3-bis(aminomethylene)succinamide moiety, and it represents the first dimer to be identified among the psammaplysin family. Data from 1D- and 2D-NMR and HRMS supported the chemical structures of the compounds. Psammaceratin A (1) and psammaplysin A (2) exhibited significant growth inhibition of HCT 116, HeLa, and MBA-MB-231 cells down to 3.1 μM. Full article
(This article belongs to the Special Issue Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents)
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Review

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75 pages, 14661 KiB  
Review
Antitumor Profile of Carbon-Bridged Steroids (CBS) and Triterpenoids
by Valery M. Dembitsky, Tatyana A. Gloriozova and Vladimir V. Poroikov
Mar. Drugs 2021, 19(6), 324; https://doi.org/10.3390/md19060324 - 03 Jun 2021
Cited by 6 | Viewed by 4222
Abstract
This review focuses on the rare group of carbon-bridged steroids (CBS) and triterpenoids found in various natural sources such as green, yellow-green, and red algae, marine sponges, soft corals, ascidians, starfish, and other marine invertebrates. In addition, this group of rare lipids is [...] Read more.
This review focuses on the rare group of carbon-bridged steroids (CBS) and triterpenoids found in various natural sources such as green, yellow-green, and red algae, marine sponges, soft corals, ascidians, starfish, and other marine invertebrates. In addition, this group of rare lipids is found in amoebas, fungi, fungal endophytes, and plants. For convenience, the presented CBS and triterpenoids are divided into four groups, which include: (a) CBS and triterpenoids containing a cyclopropane group; (b) CBS and triterpenoids with cyclopropane ring in the side chain; (c) CBS and triterpenoids containing a cyclobutane group; (d) CBS and triterpenoids containing cyclopentane, cyclohexane or cycloheptane moieties. For the comparative characterization of the antitumor profile, we have added several semi- and synthetic CBS and triterpenoids, with various additional rings, to identify possible promising sources for pharmacologists and the pharmaceutical industry. About 300 CBS and triterpenoids are presented in this review, which demonstrate a wide range of biological activities, but the most pronounced antitumor profile. The review summarizes biological activities both determined experimentally and estimated using the well-known PASS software. According to the data obtained, two-thirds of CBS and triterpenoids show moderate activity levels with a confidence level of 70 to 90%; however, one third of these lipids demonstrate strong antitumor activity with a confidence level exceeding 90%. Several CBS and triterpenoids, from different lipid groups, demonstrate selective action on different types of tumor cells such as renal cancer, sarcoma, pancreatic cancer, prostate cancer, lymphocytic leukemia, myeloid leukemia, liver cancer, and genitourinary cancer with varying degrees of confidence. In addition, the review presents graphical images of the antitumor profile of both individual CBS and triterpenoids groups and individual compounds. Full article
(This article belongs to the Special Issue Pharmacological Activity and Biomedical Potential of Marine Antitumor Agents)
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