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Marine Drugs
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Development and Application of Marine-Sourced Anti-cancer and Cancer Pain Control...
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Development and Application of Marine-Sourced Anti-cancer and Cancer Pain Control Agents

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

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 10905

Special Issue Editor

Dr. Giuseppe La Regina

E-Mail Website
Guest Editor
Dipartimento di Chimica e Tecnologie del Farmaco, Sapienza Universita’ di Roma, Piazzale Aldo Moro 5, 00185 Rome, Italy
Interests: anticancer agents; anti-infective agents; heterocyclic chemistry; small molecules; microwave-assisted organic chemistry and extraction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The marine habitat is an unlimited source of bioactive molecules with unique chemical structures. Among these, compounds endowed with anticancer activity are of particular interest, because cancer remains one of the most challenging problems for human health. In addition, people with cancer commonly suffer from pain, whose pharmacological treatment is often associated with several side effects. Even if cancer and pain therapies have been considerably improved in the last decades, there is an urgent need to identify new bioactive compounds in order to obtain more efficacious and safe drugs for people living with cancer and cancer-related pain.

For this Special Issue, “Development and Application of Marine-Sourced Anticancer and Cancer Pain Control Agents”, we invite scientists from both academia and industry to publish their recent results on new anticancer and cancer pain control agents of marine origin. The Issue will cover all aspects of chemical and pharmaceutical relevance, such us extraction, identification, structure elucidation, total synthesis, structure–activity relationships, molecular modelling simulations, pharmacological and pharmacokinetics characterization of marine compounds.

Dr. Giuseppe La Regina
Guest Editor

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

  • Cancer
  • Pain
  • Marine bioactive compounds
  • Drug
  • Human health

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Published Papers (3 papers)

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Research

18 pages, 5369 KiB  
Article
Combined Treatment of Heteronemin and Tetrac Induces Antiproliferation in Oral Cancer Cells
by Chi-Hung Huang, Tung-Yung Huang, Wong-Jin Chang, Yi-shin Pan, Hung-Ru Chu, Zi-Lin Li, Sukanya Unson, Yu-Tang Chin, Chi-Yu Lin, Haw-Ming Huang, Chao-Nan Hsiung, Fabio Gionfra, Paolo De Vito, Jens Z. Pedersen, Sandra Incerpi, Yi-Ru Chen, Sheng-Yang Lee, Hung-Yun Lin, Paul J. Davis, Jacqueline Whang-Peng and Kuan Wangadd Show full author list remove Hide full author list
Mar. Drugs 2020, 18(7), 348; https://doi.org/10.3390/md18070348 - 2 Jul 2020
Cited by 13 | Viewed by 3881
Abstract
Background: Heteronemin, a marine sesterterpenoid-type natural product, possesses an antiproliferative effect in cancer cells. In addition, heteronemin has been shown to inhibit p53 expression. Our laboratory has demonstrated that the thyroid hormone deaminated analogue, tetrac, activates p53 and induces antiproliferation in colorectal cancer. [...] Read more.
Background: Heteronemin, a marine sesterterpenoid-type natural product, possesses an antiproliferative effect in cancer cells. In addition, heteronemin has been shown to inhibit p53 expression. Our laboratory has demonstrated that the thyroid hormone deaminated analogue, tetrac, activates p53 and induces antiproliferation in colorectal cancer. However, such drug mechanisms are still to be studied in oral cancer cells. Methods: We investigated the antiproliferative effects by Cell Counting Kit-8 and flow cytometry. The signal transduction pathway was measured by Western blotting analyses. Quantitative PCR was used to evaluate gene expression regulated by heteronemin, 3,3’,5,5’-tetraiodothyroacetic acid (tetrac), or their combined treatment in oral cancer cells. Results: Heteronemin inhibited not only expression of proliferative genes and Homo Sapiens Thrombospondin 1 (THBS-1) but also cell proliferation in both OEC-M1 and SCC-25 cells. Remarkably, heteronemin increased TGF-β1 expression in SCC-25 cells. Tetrac suppressed expression of THBS-1 but not p53 expression in both cancer cell lines. Furthermore, the synergistic effect of tetrac and heteronemin inhibited ERK1/2 activation and heteronemin also blocked STAT3 signaling. Combined treatment increased p53 protein and p53 activation accumulation although heteronemin inhibited p53 expression in both cancer cell lines. The combined treatment induced antiproliferation synergistically more than a single agent. Conclusions: Both heteronemin and tetrac inhibited ERK1/2 activation and increased p53 phosphorylation. They also inhibited THBS-1 expression. Moreover, tetrac suppressed TGF-β expression combined with heteronemin to further enhance antiproliferation and anti-metastasis in oral cancer cells. Full article
(This article belongs to the Special Issue Development and Application of Marine-Sourced Anti-cancer and Cancer Pain Control Agents)
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12 pages, 1544 KiB  
Communication
The Influence of Caerulomycin A on the Intestinal Microbiota in SD Rats
by Hongwei Zhang, Mengmeng Lan, Guodong Cui and Weiming Zhu
Mar. Drugs 2020, 18(5), 277; https://doi.org/10.3390/md18050277 - 22 May 2020
Cited by 6 | Viewed by 3193
Abstract
Caerulomycin A (CRM A) is the first example of natural caerulomycins with a 2,2′-bipyridyl ring core and 6-aldoxime functional group from Streptomyces caeruleus and recently from marine-derived Actinoalloteichus cyanogriseus WH1-2216-6. Our previous study revealed that CRM A showed anti-tumor activity against human colorectal [...] Read more.
Caerulomycin A (CRM A) is the first example of natural caerulomycins with a 2,2′-bipyridyl ring core and 6-aldoxime functional group from Streptomyces caeruleus and recently from marine-derived Actinoalloteichus cyanogriseus WH1-2216-6. Our previous study revealed that CRM A showed anti-tumor activity against human colorectal cancer (CRC) both in vitro and in vivo. Because some intestinal flora can affect the occurrence and development of CRC, the influence of CRM A on the intestinal flora is worthy of study in Sprague–Dawley (SD) rats. The high throughput sequencing of the V3-V4 hypervariable region in bacterial 16S rDNA gene results showed that the CRM A affected the diversity of intestinal flora of the SD rats treated with CRM A for 2, 3 and 4 weeks. Further analysis indicated that the abundance of genera Prevotella_1, Prevotellaceae_UCG-001, and Lactobacillus were increased while the that of genera Alloprevotella and Ruminiclostridium_1 were decreased. For the CRC related intestinal flora, the abundance of genera Bacteroides, Fusobacterium, Enterococcus, Escherichia-Shigella, Klebsiella, Streptococcus, Ruminococcus_2, and Peptococcus of SD rats treated with CRM A were decreased, while that of abundance of genera Bifidobacterium, Lactobacillus, Faecalibacterium, Blautia, Oscillibacter, and Clostridium were increased. The results indicated that CRM A could influence the intestinal flora by inhibiting some species of harmful flora and improving the beneficial bacteria in intestinal flora in the SD rats. The results may provide a new idea for revealing the mechanism of the anti-CRC activity of CRM A. Full article
(This article belongs to the Special Issue Development and Application of Marine-Sourced Anti-cancer and Cancer Pain Control Agents)
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20 pages, 5393 KiB  
Article
A Natural Quinazoline Derivative from Marine Sponge Hyrtios erectus Induces Apoptosis of Breast Cancer Cells via ROS Production and Intrinsic or Extrinsic Apoptosis Pathways
by Arun Kumar De, Ramachandran Muthiyan, Samiran Mondal, Nilkamal Mahanta, Debasis Bhattacharya, Perumal Ponraj, Kangayan Muniswamy, Anandamoy Kundu, Madhu Sudhan Kundu, Jai Sunder, Dhanasekar Karunakaran, Asit Kumar Bera, Sibnarayan Dam Roy and Dhruba Malakar
Mar. Drugs 2019, 17(12), 658; https://doi.org/10.3390/md17120658 - 23 Nov 2019
Cited by 15 | Viewed by 3261
Abstract
Here, we report the therapeutic potential of a natural quinazoline derivative (2-chloro-6-phenyl-8H-quinazolino[4,3-b]quinazolin-8-one) isolated from marine sponge Hyrtios erectus against human breast cancer. The cytotoxicity of the compound was investigated on a human breast carcinoma cell line (MCF-7). Antiproliferative activity of the compound was [...] Read more.
Here, we report the therapeutic potential of a natural quinazoline derivative (2-chloro-6-phenyl-8H-quinazolino[4,3-b]quinazolin-8-one) isolated from marine sponge Hyrtios erectus against human breast cancer. The cytotoxicity of the compound was investigated on a human breast carcinoma cell line (MCF-7). Antiproliferative activity of the compound was estimated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. MTT assay showed significant inhibition of MCF-7 cells viability with the IC50 value of 13.04 ± 1.03 µg/mL after 48 h. The compound induced down-regulation of anti-apoptotic Bcl-2 protein and increase in the pro-apoptotic Bax/Bcl-2 ratio in MCF-7 cells. The compound activated the expression of Caspases-9 and stimulated downstream signal transducer Caspase-7. In addition, Caspase-8 showed remarkable up-regulation in MCF-7 cells treated with the compound. Moreover, the compound was found to promote oxidative stress in MCF-7 cells that led to cell death. In conclusion, the compound could induce apoptosis of breast carcinoma cells via a mechanism that involves ROS production and either extrinsic or intrinsic apoptosis pathways. The systemic toxic potential of the compound was evaluated in an in vivo mouse model, and it was found non-toxic to the major organs. Full article
(This article belongs to the Special Issue Development and Application of Marine-Sourced Anti-cancer and Cancer Pain Control Agents)
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