Curcumin in gastric cancer treatment: A commentary on mechanistic insights and future directions

Abstract

The study by Yang et al presents a comprehensive investigation into the therapeutic potential of curcumin for gastric cancer (GC). Using network pharmacology, the researchers identified 48 curcumin-related genes, 31 of which overlap with GC targets. Key genes, including ESR1, EGFR, CYP3A4, MAPK14, CYP1A2, and CYP2B6, are linked to poor survival in GC patients. Molecular docking confirmed strong binding affinity of curcumin to these genes. In vitro experiments demonstrated that curcumin effectively inhibits the growth and proliferation of BGC-823, suggesting its therapeutic potential in GC through multiple targets and pathways.

Key Words: Curcumin; Gastric cancer; Network pharmacology; Mechanism of action; In vitro experiments

Core Tip: The study by Yang et al elucidates the therapeutic mechanisms of curcumin in gastric cancer treatment, identifying key targets and confirming their interactions with curcumin through molecular docking. This study provides a solid foundation for further exploration of curcumin’s role in gastric cancer therapy.

TO THE EDITOR

We had the privilege of reading the article “Curcumin for gastric cancer: Mechanism prediction via network pharmacology, docking, and in vitro experiments[1],” authored by Yang et al[1], published in the World Journal of Gastrointestinal Oncology. This study explores the potential therapeutic mechanisms of curcumin for gastric cancer (GC) through network pharmacology, molecular docking, and in vitro experiments, offering new perspectives and approaches for GC treatment.

We would like to commend the authors for their work on elucidating the pharmacological mechanisms of curcumin. The article initially assesses the pharmacokinetic properties of curcumin using network pharmacology methods and predicts its potential targets through various databases. The cross-analysis with GC disease targets successfully identified multiple key genes associated with curcumin, laying the foundation for subsequent experimental validation, and providing a powerful tool for the modernization of research into natural medicinal materials. The identification of key genes such as ESR1 and EGFR, along with the validation of curcumin’s binding affinity through molecular docking, presents a significant advancement in the field[2,3].

It is particularly noteworthy that this study goes beyond theoretical exploration and further verifies the interaction between curcumin and core targets through molecular docking and in vitro experiments. The inhibitory effects of curcumin on BGC-823 cells contribute to further evidence for the use of curcumin in cancer therapy[4]. The highlight of this study lies in its integration of multidisciplinary methods. By employing advanced network pharmacology, combined with molecular docking techniques and in vitro experimental validation, this interdisciplinary research approach provides a new strategy to explore the pharmacological effects of natural medicinal materials. Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis reveal that curcumin may act through multiple biological processes and signaling pathways. Furthermore, the analysis of patient survival data using Kaplan–Meier plots shows that high expression of certain core targets is correlated with poor prognosis in GC patients, providing clinical relevance for curcumin as a potential therapeutic agent.

However, we also have some exploratory opinions on certain aspects of the study. Firstly, regarding the pharmacokinetic properties of curcumin, although the article mentions the assessment results of Lipinski’s Rule of Five, the discussion on the bioavailability and pharmacokinetic characteristics of curcumin in the body appears insufficient. Given that the bioavailability of curcumin has always been one of the challenges in its clinical application[5], future research that further explores its pharmacokinetic behavior in the body will be significant in promoting its clinical use.

Secondly, while the study’s network pharmacology predicted multiple targets and validated them through molecular docking experiments, an in-depth discussion on the specific mechanisms by which these targets affect the occurrence and development of GC and how they synergistically influence the biological behavior of GC cells seems lacking. Future research that delves into the molecular mechanisms of action of these core targets will help to better understand the anti-cancer effects of curcumin.

In future experiments, the range of curcumin concentrations used in the article may need further optimization in animal models to simulate real clinical use and consider drug interactions and side effects. The study should also consider the potential genetic and epigenetic differences between patients, which may affect the efficacy and tolerance of curcumin. Lastly, although the in vitro experimental results are encouraging, the anti-cancer effects and mechanisms of curcumin in the body still need to be verified by more in vivo experiments. It is suggested that the authors consider conducting relevant animal model studies to further explore the in vivo anti-tumor effects of curcumin.

In summary, the research by Yang et al[1] provides valuable insights and directions for the application of curcumin in GC treatment. We commend this work and look forward to the authors conducting more in-depth investigations on the issues in their future studies.

ACKNOWLEDGEMENTS

We express our gratitude to the reviewers for their constructive feedback, which has significantly enhanced the quality of this manuscript.