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Marine Bioactive Compounds: Roles in Signaling Pathway Regulation and Potential Applications

A special issue of Marine Drugs (ISSN 1660-3397). This special issue belongs to the section "Marine Pharmacology".

Deadline for manuscript submissions: closed (15 June 2026) | Viewed by 2050

Editor

Department of Oriental Pharmacy, College of Pharmacy, Woosuk University, Wanju 55338, Jeonbuk, Republic of Korea
Interests: pharmaceutical; anti-cancer agents; immunomodulatory; natural products; signaling pathway
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,                

Marine ecosystems represent an extraordinary reservoir of structurally diverse bioactive compounds that have evolved to interact with complex biological systems. These marine-derived molecules exhibit remarkable potential in modulating intracellular signaling pathways that regulate key physiological and pathological processes, including inflammation, oxidative stress, immune regulation, and cancer progression.

This Special Issue, Marine Bioactive Compounds: Roles in Signaling Pathway Regulation and Potential Applications”, aims to highlight the latest advances in understanding how marine natural products influence cellular signaling networks and contribute to therapeutic development. We particularly welcome studies exploring molecular mechanisms of action, signaling pathway modulation, and cross-talk among key regulators.

We invite review papers and original articles that integrate molecular pharmacology, omics technologies, computational modeling, and in vivo studies to explore how marine compounds influence key signaling networks. Articles addressing their roles in disease prevention, drug resistance modulation, and novel therapeutic strategies are particularly encouraged.

Dr. Ji-Hye Ahn
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • marine bioactive compounds
  • natural products
  • signaling pathway regulation
  • molecular mechanisms of action
  • inflammation
  • oxidative stress
  • cancer
  • network pharmacology
  • translational marine pharmacology

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Published Papers (2 papers)

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Research

19 pages, 3571 KB  
Article
Marine-Derived Fungal Metabolite MHO7 Promotes Breast Cancer Apoptosis as a Hippo Pathway Regulator by Modulating the YAP-TEAD Axis
by Xue Ren, Linfei Wang, Yuxuan Huang, Bei Shu, Kerui Hou, Mengyao Chen, Yao Xiao, Jiahong Liang, Hao Yan, Shuaishuai Ding, Hui Qiu, Jin Lu, Kui Hong and Xin Liu
Mar. Drugs 2026, 24(8), 273; https://doi.org/10.3390/md24080273 - 6 Aug 2026
Abstract
Breast cancer, especially triple-negative breast cancer (TNBC) and endocrine-resistant disease, remains difficult to treat because of limited effective targeted therapies. In this study, we evaluated the antitumor activity and potential mechanism of MHO7, a marine-derived ophiobolin metabolite, in ER-positive ZR-75-30 cells, tamoxifen-resistant LCC2 [...] Read more.
Breast cancer, especially triple-negative breast cancer (TNBC) and endocrine-resistant disease, remains difficult to treat because of limited effective targeted therapies. In this study, we evaluated the antitumor activity and potential mechanism of MHO7, a marine-derived ophiobolin metabolite, in ER-positive ZR-75-30 cells, tamoxifen-resistant LCC2 cells, and TNBC MDA-MB-231 models. MHO7 dose-dependently reduced cell viability, wound closure, and clonogenic growth in ZR-75-30 and LCC2 cells, with IC50 values of 11.53 and 10.43 μM, respectively. MHO7 also promoted apoptotic cell death, accompanied by increased reactive oxygen species accumulation and altered expression of apoptosis-related proteins, including Bcl-2 and caspase-3. N-acetyl-L-cysteine partially attenuated MHO7-induced apoptosis and YAP reduction in MDA-MB-231 cells, suggesting a contribution of oxidative stress. Molecular docking predicted that MHO7 could occupy the conserved TEAD palmitoylation pocket, and subsequent in vitro analyses showed suppression of YAP/TAZ-TEAD signaling, including reduced YAP nuclear accumulation and decreased TEAD4 expression. In an MDA-MB-231 xenograft model, MHO7 significantly inhibited tumor growth, reduced CD31-positive microvessel density, and decreased Hippo pathway-related transcriptional readouts. These findings indicate that MHO7 exerts broad antitumor activity in breast cancer models through oxidative stress-associated apoptosis and modulation of YAP/TAZ-TEAD signaling, supporting its further development as a lead compound for treatment-resistant breast cancer. Full article
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22 pages, 3592 KB  
Article
Phlorotannins from Ecklonia cava Regulate Dual Signaling Pathways, IL-17RA/Act1 and ERK1/2, to Suppress Ovarian Cancer Progression and Tumor-Associated Macrophage Activation
by Eun-Hye Kim, Hwi-Ho Lee, Jung-Hye Choi and Ji-Hye Ahn
Mar. Drugs 2026, 24(1), 12; https://doi.org/10.3390/md24010012 - 24 Dec 2025
Cited by 2 | Viewed by 1632
Abstract
Background: Marine-derived secondary metabolites such as phlorotannins from the edible brown alga Ecklonia cava exhibit diverse bioactivities. However, their mechanisms in inflammation-associated cancer remain insufficiently understood. Methods: This study explored the anticancer potential of three major phlorotannins (dieckol, 7-phloroeckol, and 8,8′-bieckol) through network [...] Read more.
Background: Marine-derived secondary metabolites such as phlorotannins from the edible brown alga Ecklonia cava exhibit diverse bioactivities. However, their mechanisms in inflammation-associated cancer remain insufficiently understood. Methods: This study explored the anticancer potential of three major phlorotannins (dieckol, 7-phloroeckol, and 8,8′-bieckol) through network pharmacology, molecular docking, molecular dynamics simulations, and in vitro validation in SKOV3 ovarian cancer cells and tumor-associated macrophages (TAMs). Results: Computational analyses revealed stable binding of phlorotannins to IL-17RA, with 7-phloroeckol and 8,8′-bieckol preferentially engaging loop-proximal regions of the receptor, while dieckol interacted with spatially distinct residues. In SKOV3 ovarian cancer cells, phlorotannins suppressed migration and invasion by approximately 40 to 60%, accompanied by reduced MMP expression linked to IL-17RA–Act1 signaling attenuation and by increased TIMP1 expression in association with transient ERK1/2 activation. In TAMs, phlorotannins attenuated pro-tumorigenic cytokine production and polarization marker expression, indicating suppression of tumor-supportive immune activity. Conclusions: Collectively, these findings demonstrate that E. cava-derived phlorotannins exert anti-metastatic effects through dual regulation of IL-17RA/Act1 and ERK1/2 signaling pathways, offering mechanistic insight into their therapeutic potential against inflammation-driven malignancies. Full article
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