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Marine Drugs
Special Issues
Marine Natural Products as Regulators in Cell Signaling Pathway
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Marine Natural Products as Regulators in Cell Signaling Pathway

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

Deadline for manuscript submissions: 30 June 2025 | Viewed by 2443

Special Issue Editor

Dr. Faliang An

E-Mail Website
Guest Editor
State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, 130 Meilong Road, Shanghai 200237, China
Interests: drug development; natural products; metabolic pathway regulation; microbial fermentation optimization; bioactivity screening; pharmacological mechanisms

Special Issue Information

Dear Colleagues,

Marine natural products have attracted growing interest in recent years as modulators of cell signaling pathways. These compounds exhibit distinct biological activities, effectively influencing intracellular signal transduction processes and regulating key cellular functions such as proliferation, differentiation, and apoptosis. Investigating the effects of marine natural products on these signaling pathways offers significant insights into their underlying pharmacological mechanisms, providing a solid foundation for the development of novel therapeutic strategies. With the advancement of cutting-edge molecular biology techniques, including genomics, proteomics, and cell signaling analysis, significant strides have been made in this area of research. Notably, marine natural products have demonstrated considerable therapeutic potential, particularly in the treatment of cancer, inflammation, and various other diseases.

We invite researchers to submit original research and review articles on marine natural products, with a particular emphasis on the following topics:

  • The regulatory effects of marine natural products on cell signaling pathways;
  • The role of marine natural products in disease models and their potential for clinical application;
  • The identification of key targets and biomarkers within cell signaling pathways;
  • The structure–activity relationship of marine natural products.

Dr. Faliang An
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

  • marine-derived natural products
  • cell signaling pathways
  • biological activities
  • pharmacological mechanisms
  • therapeutic strategies
  • structure–activity relationship

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

18 pages, 10369 KiB  
Article
TMF Attenuates Cognitive Impairment and Neuroinflammation by Inhibiting the MAPK/NF-κB Pathway in Alzheimer’s Disease: A Multi-Omics Analysis
by Yonglin Liu, Xi Xu, Xiaoming Wu, Guodong Yang, Jiaxin Luo, Xinli Liang, Jie Chen and Yiguang Li
Mar. Drugs 2025, 23(2), 74; https://doi.org/10.3390/md23020074 - 7 Feb 2025
Viewed by 925
Abstract
The rising prevalence of Alzheimer’s disease (AD) underscores the urgent need for novel therapeutic agents derived from natural sources. Among flavonoids, 3′,4′,5,7-tetramethoxyflavone (TMF), a structural analog of luteolin, has gained attention for its favorable pharmacokinetics and potential neuroprotective properties. Despite the significant neuroprotective [...] Read more.
The rising prevalence of Alzheimer’s disease (AD) underscores the urgent need for novel therapeutic agents derived from natural sources. Among flavonoids, 3′,4′,5,7-tetramethoxyflavone (TMF), a structural analog of luteolin, has gained attention for its favorable pharmacokinetics and potential neuroprotective properties. Despite the significant neuroprotective effects and favorable pharmacokinetics of TMF, its efficacy and mechanism of action in AD remain unclear. This study explored TMF’s pharmacological effects in AD models, highlighting its ability to improve memory and cognitive deficits in APP/PS1 mice. TMF reduced Aβ plaques, NFTs formation, and glial activation while suppressing neuroinflammation through the MAPK/NF-κB pathway. Further analysis in LPS-induced BV2 cells revealed TMF’s ability to reduce microglial activation. These findings highlight the anti-neuroinflammatory activity of TMF, suggesting its potential as a treatment for AD. Full article
(This article belongs to the Special Issue Marine Natural Products as Regulators in Cell Signaling Pathway)
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17 pages, 9218 KiB  
Article
Blockade of the STAT3/BCL-xL Axis Leads to the Cytotoxic and Cisplatin-Sensitizing Effects of Fucoxanthin, a Marine-Derived Carotenoid, on Human Bladder Urothelial Carcinoma Cells
by Wen-Chyi Dai, Tzu-Hsuan Chen, Tzu-Ching Peng, Yung-Ching He, Chao-Yu Hsu and Chia-Che Chang
Mar. Drugs 2025, 23(2), 54; https://doi.org/10.3390/md23020054 - 22 Jan 2025
Viewed by 1301
Abstract
Bladder cancer is a globally prevalent urological malignancy, with transitional carcinoma (TCC) representing the majority of cases. Cisplatin is the primary drug for metastatic bladder cancer chemotherapy; however, its application is limited by nephrotoxicity and resistance. Signal Transducer and Activator of Transcription 3 [...] Read more.
Bladder cancer is a globally prevalent urological malignancy, with transitional carcinoma (TCC) representing the majority of cases. Cisplatin is the primary drug for metastatic bladder cancer chemotherapy; however, its application is limited by nephrotoxicity and resistance. Signal Transducer and Activator of Transcription 3 (STAT3) is an oncogenic transcription factor often overactivated in various cancers, making it an appealing drug target. Fucoxanthin, a marine carotenoid, has significant anticancer properties. This study explored Fucoxanthin’s cytotoxic effects and its potential to potentiate the efficacy of Cisplatin, along with the mechanisms underlying these effects, on human bladder TCC cells. We demonstrated that Fucoxanthin is cytotoxic to bladder TCC cells by inducing apoptosis, evidenced by z-VAD-fmk-mediated annulment of Fucoxanthin’s cytotoxicity. Furthermore, Fucoxanthin reduced the levels of inherent or interleukin-6-induced tyrosine 705-phosphorylated STAT3 accompanied by downregulating BCL-xL, a well-established STAT3 target. Notably, ectopic expression of STAT3-C, a dominant-active STAT3 mutant, or BCL-xL thwarted Fucoxanthin’s proapoptotic and cytotoxic actions. Moreover, Fucoxanthin at subtoxic dosages enhanced the susceptibility to Cisplatin-induced apoptosis of bladder TCC cells initially resistant to Cisplatin. Remarkably, this Cisplatin-sensitizing effect of Fucoxanthin was abrogated when cells ectopically expressed STAT3-C or BCL-xL. Overall, for the first time, we proved that the proapoptotic, cytotoxic, and Cisplatin-sensitizing effects of Fucoxanthin on human bladder TCC cells are attributed to the blockade of the STAT3/BCL-xL axis. Our findings highlight that targeting the STAT3/BCL-xL axis is a promising strategy to eliminate bladder TCC cells and facilitate Cisplatin sensitization, and further support the potential of incorporating Fucoxanthin into Cisplatin-based chemotherapy for treating bladder cancer. Full article
(This article belongs to the Special Issue Marine Natural Products as Regulators in Cell Signaling Pathway)
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