Synergistic inhibition of gastric cancer cell proliferation by concanavalin A and silibinin via attenuation of the JAK/STAT3 signaling pathway and molecular docking analysis

Q: What is the main objective of combining concanavalin A and silibinin in this study?

To assess whether Concanavalin A and silibinin synergistically inhibit AGS gastric cancer cell growth by attenuating the JAK/STAT3 signaling pathway.

Q: How was cell cytotoxicity and ROS generation measured?

Cytotoxicity was evaluated using the MTT assay, while ROS generation was measured using DCFH-DA staining.

Q: What apoptosis and signaling changes were observed with the combined treatment?

Combined Con-A and SB increased apoptotic signals, including Bax overexpression, Bcl-2 downregulation, caspase-3 activation, and substantial ROS generation, with a reported IC50 of 10.37 μM.

Sep 24, 2026

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Study evaluates combined natural compounds Concanavalin A (Con-A) and silibinin (SB) as a strategy to suppress gastric cancer growth. Experiments tested inhibition of AGS cell proliferation by blocking JAK/STAT3 signaling, using MTT for cytotoxicity, ROS detection with DCFH-DA staining, apoptosis assessment via AO/EtBr staining, and MMP measurement by fluorescence assays. Flow cytometry and western blotting quantified cell cycle and apoptosis markers. Results show dose-dependent cytotoxicity and pronounced apoptosis with Bax upregulation, Bcl-2 downregulation, caspase-3 activation, and elevated ROS, with synergy yielding an IC50 of 10.37 μM.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages18

Reading Time45 min

AccessFree to download

Abstract

Background

Objectives

Materials and methods

Results

Conclusion

Keywords

Hua et al. Hereditas (2025) 162:73 [https://doi.org/10.1186/s41065-025-00438-z](https://doi.org/10.1186/s41065-025-00438-z) Hereditas RESEARCH Open Access Synergistic inhibition of gastric cancer cell proliferation by concanavalin A and silibinin via attenuation of the JAK/STAT3 signaling pathway and molecular docking analysis Gaoyan Hua1†, Lisha Zhao2†, Xianjing Zeng3 and Liang Luo4* Abstract Background In the current period of pharmaceutical discovery, herbal remedies have shown to be an unmatched supply of anticancer medications. Plants and their derivatives, through analogues, play a vital role in cancer treatment. Objectives The current investigation assessed the effectiveness of inhibiting the growth of gastric cancer cells in AGS cells by blocking the JAK/ STAT3 signalling pathways using the natural medicines Concanavalin A (Con-A) and silibinin (SB) . Materials and methods After being exposed to various doses of concanavalin A, and silibinin (Con-A + SB) for 24 h (0-60 µM), the cells were evaluated for multiple studies. The MTT assay was used to examine the combination of Con-A + SB-induced cytotoxicity. To evaluate ROS, DCFH-DA staining was utilized. Dual (AO/EtBr) staining was performed to examine apoptotic modifications, and MMP levels in AGS cells were examined using the appropriate fluorescence staining assays. By using flow cytometry and western blotting, cell cycle, and apoptosis were assessed. Results The relative cytotoxicity of Con-A and SB was found to be approximately 19.6 μM and 16.78 μM,(p < 0. 05) correspondingly, according to the findings. After a 24-h incubation period, the combination of Con-A and SB generates significant cytotoxicity in AGS cells, with an IC50 of 10.37 μM (p < 0.01) . Furthermore, AGS cells treated with Con-A and SB concurrently showed increased apoptotic signals, exhibited by Bax overexpression, Bcl-2 downregulation, and Caspase-3 activation, as well as considerable ROS generation. Conclusion Therefore, the combination usage of Con-A + SB has the potential to serve as a chemotherapeutic agent since it prevents the synthesis of JAK/STAT3 intermediated control of proliferation and cell cycle-regulating proteins. Keywords Concanavalin A, Silibinin, Cell proliferation, JAK/STAT3, Gastric cancer †Gaoyan Hua and Lisha Zhao co-first authors, and contributed equally to this work. *Correspondence: Liang Luo [luoliang1364706@outlook.com](luoliang1364706@outlook.com) Full list of author information is available at the end of the article © The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/licenses/by/4.0/](http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ()[. The Creative Commons Public Domain Dedication waiver (](http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ()[http://creativecom](http://creativecom)[mons.org/publicdomain/zero/1.0/](mons.org/publicdomain/zero/1.0/)) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Hua et al. Hereditas (2025) 162:73 Background Carcinoma was formerly thought to be intractable, but

FAQs

What is the main objective of combining concanavalin A and silibinin in this study?

To assess whether Concanavalin A and silibinin synergistically inhibit AGS gastric cancer cell growth by attenuating the JAK/STAT3 signaling pathway.

How was cell cytotoxicity and ROS generation measured?

Cytotoxicity was evaluated using the MTT assay, while ROS generation was measured using DCFH-DA staining.

What apoptosis and signaling changes were observed with the combined treatment?

Combined Con-A and SB increased apoptotic signals, including Bax overexpression, Bcl-2 downregulation, caspase-3 activation, and substantial ROS generation, with a reported IC50 of 10.37 μM.

Sep 24, 2026

Uploaded by Putri