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Natural Products and Modern Drug Discovery: Emerging Strategies Targeting Cancer-...
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Natural Products and Modern Drug Discovery: Emerging Strategies Targeting Cancer- and Disease-Related Molecular Mechanisms

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 4648

Special Issue Editor

Prof. Dr. Chia-Jui Weng

E-Mail Website
Guest Editor
Department of Food & Beverage Services and Master Degree Program of Applied Living Science, Tainan University of Technology, Tainan City, Taiwan
Interests: hepatocarcinoma; natural bioactives and phytochemicals; cancer invasion and metastasis; single nucleotide polymorphism; anti-aging

Special Issue Information

Dear Colleagues,

Natural products have been at the heart of drug discovery for centuries, serving as both therapeutic agents and blueprints for the development of novel drugs. With advances in analytical chemistry, biosynthetic engineering, and computational tools, the exploration and development of natural products have entered a new era—where traditional knowledge meets modern innovation. This Special Issue focuses on the utilization and development of natural products as a foundation for modern drug discovery, particularly in addressing the molecular mechanisms underlying cancer and other diseases. We aim to highlight the latest research on how natural compounds are identified, modified, and optimized through innovative technologies to become effective, targeted therapeutics.

We invite submissions in areas including, but not limited to, the following:

  • Isolation, structural elucidation, and bioactivity profiling of novel natural products.
  • Strategies for sourcing and screening natural compounds (e.g., microbial, marine, and plant-based).
  • Biosynthetic pathway engineering and synthetic biology approaches.
  • Semisynthetic and total synthesis of natural product derivatives.
  • Structure–activity relationship (SAR) studies of natural molecules.
  • Natural product libraries and high-throughput screening platforms.
  • Integration of AI, molecular docking, or pharmacophore modeling in natural product-based design.
  • Role of natural products in overcoming drug resistance or targeting novel disease mechanisms.

This Special Issue aims to showcase how nature-inspired molecules continue to inspire the development of next-generation therapeutics, as well as how cutting-edge techniques are expanding their therapeutic potential.

We welcome original research articles, reviews, and perspective pieces that contribute to the scientific advancement of natural product-based drug discovery.

Prof. Dr. Chia-Jui Weng
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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life 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 2600 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

  • natural products
  • phytochemicals
  • drug discovery
  • bioactivity profiling
  • pharmacophore modeling
  • synthetic biology
  • cancer therapy
  • microbial metabolites

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

Published Papers (3 papers)

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Research

15 pages, 1887 KB  
Article
Hyperoside Stabilizes Redox–Mitochondrial–Inflammatory Networks in a Haloperidol-Induced Tardive Dyskinesia–Like Model
by Hsiang-Chien Tseng, Mao-Hsien Wang, Kuo-Chi Chang and Chih-Pei Hsu
Life 2026, 16(5), 814; https://doi.org/10.3390/life16050814 (registering DOI) - 13 May 2026
Viewed by 107
Abstract
Tardive dyskinesia (TD) is a persistent hyperkinetic movement disorder associated with prolonged dopamine D2 receptor blockade, particularly during chronic haloperidol (HP) exposure. Emerging evidence suggests that TD-like pathology is sustained by an interconnected redox–mitochondrial–inflammatory network within striatal circuits; however, the regulatory architecture of [...] Read more.
Tardive dyskinesia (TD) is a persistent hyperkinetic movement disorder associated with prolonged dopamine D2 receptor blockade, particularly during chronic haloperidol (HP) exposure. Emerging evidence suggests that TD-like pathology is sustained by an interconnected redox–mitochondrial–inflammatory network within striatal circuits; however, the regulatory architecture of this network remains incompletely defined. Hyperoside (HS), a flavonol glycoside with cytoprotective properties, has been implicated in cellular stress-response modulation, yet its role in antipsychotic-induced motor dysfunction remains unclear. In this study, a six-group mechanistic design was employed in which rats received HP (1 mg/kg, i.p., 21 days) to induce TD-like orofacial dyskinesia (OD), quantified by vacuous chewing movements (VCMs) and tongue protrusions (TPs). HS (30 mg/kg, i.p.) was administered alone or in combination with HP, with or without pharmacological inhibition of nuclear factor erythroid 2–related factor 2 (Nrf2) using ML385. HP exposure induced progressive dyskinetic behavior accompanied by oxidative and nitrosative stress, mitochondrial dysfunction, increased pro-inflammatory cytokines, and elevated caspase-3 activity in the striatum. HS significantly attenuated behavioral abnormalities while restoring redox balance, preserving mitochondrial enzyme activities, and reducing inflammatory and apoptotic signaling. Notably, Nrf2 inhibition intensified molecular pathology without proportionally worsening behavioral outcomes, indicating a dissociation between biochemical vulnerability and overt motor expression. Furthermore, ML385 markedly attenuated HS-mediated protection across multiple endpoints. Collectively, these findings support a potential protective role for Nrf2-related regulatory mechanisms in limiting network destabilization in TD-like pathology, while highlighting the importance of integrated stress-response pathways in modulating disease progression. Full article
(This article belongs to the Special Issue Natural Products and Modern Drug Discovery: Emerging Strategies Targeting Cancer- and Disease-Related Molecular Mechanisms)
15 pages, 4167 KB  
Article
Erucin Targets Oncogenic Signaling Pathways in Triple-Negative Breast Cancer: An Integrated Network Pharmacology and In Vitro Study
by Humera Banu, Eyad Al Shammari, Husam Qanash, Mitesh Patel, Mohd Adnan, Syed Shahanawaz, Mohammad Idreesh Khan, Malak Yahia Qattan and Syed Amir Ashraf
Life 2026, 16(5), 708; https://doi.org/10.3390/life16050708 - 22 Apr 2026
Viewed by 386
Abstract
This study aims to investigate the potential anticancer effects of erucin, an isothiocyanate derived from Eruca sativa, in triple-negative breast cancer (TNBC) by predicting molecular targets and evaluating its in vitro effects on TNBC cell proliferation, apoptosis and cell cycle distribution. Potential [...] Read more.
This study aims to investigate the potential anticancer effects of erucin, an isothiocyanate derived from Eruca sativa, in triple-negative breast cancer (TNBC) by predicting molecular targets and evaluating its in vitro effects on TNBC cell proliferation, apoptosis and cell cycle distribution. Potential protein targets of erucin were identified using SwissTargetPrediction, resulting in 117 targets, of which 84 overlapped with TNBC-related genes sourced from GeneCards, DisGeNET, and OMIM. Protein–protein interaction analysis was performed to identify key hub genes. In vitro experiments were conducted using MDA-MB-231 TNBC cells to assess dose-dependent effects on cell viability. Flow cytometry was employed to evaluate apoptotic cell populations and cell cycle distribution. Protein–protein interaction analysis identified ten hub genes, including AKT1, STAT3, EGFR, and MMP9, representing highly connected nodes within the predicted interaction network. In vitro studies showed dose-dependent reduction in MDA-MB-231 cell viability following erucin treatment, with an IC50 of approximately 48.87 µg/mL. Flow cytometry revealed increased apoptotic cell population and G1 phase accumulation. These findings suggest that erucin is associated with cytotoxic and antiproliferative effects in TNBC cells and may interact with multiple cancer-related targets. However, the identified molecular targets and pathways are based on computational predictions and require further experimental validation. Overall, this study provides a preliminary integrated framework linking computational predictions with experimental observations, which may support future mechanistic and preclinical investigations of erucin in TNBC. Full article
(This article belongs to the Special Issue Natural Products and Modern Drug Discovery: Emerging Strategies Targeting Cancer- and Disease-Related Molecular Mechanisms)
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16 pages, 2491 KB  
Article
Gut Microbiota Modulation and Anti-Obesity Potential of Epigallocatechin-3-Gallate-Quercetin-Rutin Against High-Fat Diet-Induced Obesity in Rats
by Yu-Jou Chien, Ching-Chang Cho, Yu-Ting Hung, Li-You Chen, Yue-Ching Wong, Shiuan-Chih Chen and Chin-Lin Hsu
Life 2025, 15(8), 1331; https://doi.org/10.3390/life15081331 - 21 Aug 2025
Cited by 2 | Viewed by 1825
Abstract
Polyphenols have been widely recognized for their potential anti-obesity effects. This study aimed to evaluate the impact of a polyphenol compound-epigallocatechin-3-gallate, quercetin, and rutin (EQR) on obesity-related parameters and gut microbiota composition. After four weeks of high-fat diet (HFD) induction, the obese Wistar [...] Read more.
Polyphenols have been widely recognized for their potential anti-obesity effects. This study aimed to evaluate the impact of a polyphenol compound-epigallocatechin-3-gallate, quercetin, and rutin (EQR) on obesity-related parameters and gut microbiota composition. After four weeks of high-fat diet (HFD) induction, the obese Wistar male rats received EQR treatment for an additional four weeks. EQR supplementation significantly reduced body weight gain, feed efficiency, adipose tissue accumulation, and liver lipid content in obese rats. Additionally, it enhanced fecal short-chain fatty acid (SCFA) levels and modulated gut microbiota composition. Specifically, EQR treatment significantly induced Fusobacteria, Fusobacteriaceae, Christensenellaceae, Christensenellaceae R-7 group, Lachnoclostridium, Enterorhabdus, and Parvibacter levels and reduced Deferribacteres and Mucispirillum levels. Gene expression analysis in liver, white adipose tissue (WAT), and brown adipose tissue (BAT) revealed that EQR upregulated the expression of liver PPAR-α, WAT SIRT-1, and BAT PGC-1α, while downregulating liver PPAR-γ, liver FATP-1, and WAT FAS, indicating its role in promoting fatty acid oxidation and thermogenesis, as well as suppressing lipid synthesis and transport. In conclusion, EQR demonstrated significant anti-obesity effects by modulating gut microbiota and lipid metabolism, suggesting its potential as a functional ingredient for obesity management. Full article
(This article belongs to the Special Issue Natural Products and Modern Drug Discovery: Emerging Strategies Targeting Cancer- and Disease-Related Molecular Mechanisms)
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