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Antioxidants
Volume 14
Issue 6
10.3390/antiox14060694
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Article

Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway

by
Zhibin Liu
1,
Ke Huang
1,
Hai Huang
2,
Eungyung Kim
3,
Hyeonjin Kim
1,
Chae Yeon Kim
1,
Dong Joon Kim
4,
Sang In Lee
1,
Sangsik Kim
5,6,
Do Yoon Kim
7,
Kangdong Liu
8,
Zae Young Ryoo
9,
Mee-Hyun Lee
10,
Lei Ma
1,* and
Myoung Ok Kim
1,*
1
Department of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju-si 37224, Gyeongsang buk-do, Republic of Korea
2
Henan International Joint Laboratory of TCM Syndrome and Prescription in Signaling, Traditional Chinese Medicine (Zhong Jing) School, Henan University of Chinese Medicine, Zhengzhou 450046, China
3
Department of Oral and Maxillofacial Surgery, School of Dentistry, University of Texas Health Science Cente at San Antonio, San Antonio, TX 78229, USA
4
Department of Microbiology, College of Medicine, Dankook University, Cheonan 31116, Chungcheongnam-do, Republic of Korea
5
Department of Energy Chemical Engineering, Kyungpook National University, Sangju-si 37224, Gyeongsang buk-do, Republic of Korea
6
Convergence Research Center of Mechanical and Chemical Engineering, Kyungpook National University, 2559 Gyeongsang-daero, Sangju-si 37224, Gyeongsang buk-do, Republic of Korea
7
Gyeongsangbukdo Livestock Research Institute, Yeongju 36052, Gyeongsang buk-do, Republic of Korea
8
China–US (Henan) Hormel Cancer Institute, Zhengzhou 450008, China
9
BK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, Kyungpook National University, Daegu 41566, Gyeongsang buk-do, Republic of Korea
10
Korean Medicine Research Center for Bi-Wi Control Based Gut-Brain System Regulation, College of Korean Medicine, Dongshin University, Naju-si 58245, Jeollanam-do, Republic of Korea
*
Authors to whom correspondence should be addressed.
Antioxidants 2025, 14(6), 694; https://doi.org/10.3390/antiox14060694 (registering DOI)
Submission received: 7 April 2025 / Revised: 26 May 2025 / Accepted: 4 June 2025 / Published: 8 June 2025
(This article belongs to the Special Issue Redox Signaling in Cancer: Mechanisms and Therapeutic Opportunities)
Versions Notes

Abstract

Esophageal squamous cell carcinoma (ESCC), one of the most frequent malignant tumors of the digestive system, is marked by a poor prognosis and high mortality rate. There is a critical need for effective therapeutic strategies with minimal side effects. Isoquercitrin (IQ) is a natural compound with potent antioxidant properties in cancer and cardiovascular diseases. However, its specific effects and mechanisms in ESCC remain largely unexplored. This study aims to investigate the effects of IQ in ESCC cells and elucidate the mechanisms underlying its therapeutic effects. Specifically, its impact on cell proliferation, colony formation, migration, and invasion was assessed using cell viability assay, morphology, transwell, and colony formation assays. The effects on apoptosis were evaluated by flow cytometry, while immunofluorescence (IF) staining and Western blotting were performed to confirm the underlying mechanisms. The in vivo anti-cancer effects of IQ were then evaluated using a xenograft tumor model. Our results demonstrate that IQ inhibits ESCC cell growth and colony formation while promoting its apoptosis by enhancing caspase activation and downregulating Bcl-2 expression. Furthermore, IQ suppresses cell migration by modulating the epithelial–mesenchymal transition-related proteins. Additionally, IQ induces excessive autophagy by promoting reactive oxygen species accumulation and inhibiting the AKT/mTOR signaling pathway. Importantly, IQ effectively reduces tumor growth in vivo, highlighting its potential as a therapeutic agent for ESCC.
Keywords: esophageal squamous cell carcinoma; AKT/mTOR; anti-cancer; excessive autophagy; apoptosis esophageal squamous cell carcinoma; AKT/mTOR; anti-cancer; excessive autophagy; apoptosis

Share and Cite

MDPI and ACS Style

Liu, Z.; Huang, K.; Huang, H.; Kim, E.; Kim, H.; Kim, C.Y.; Kim, D.J.; Lee, S.I.; Kim, S.; Kim, D.Y.; et al. Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway. Antioxidants 2025, 14, 694. https://doi.org/10.3390/antiox14060694

AMA Style

Liu Z, Huang K, Huang H, Kim E, Kim H, Kim CY, Kim DJ, Lee SI, Kim S, Kim DY, et al. Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway. Antioxidants. 2025; 14(6):694. https://doi.org/10.3390/antiox14060694

Chicago/Turabian Style

Liu, Zhibin, Ke Huang, Hai Huang, Eungyung Kim, Hyeonjin Kim, Chae Yeon Kim, Dong Joon Kim, Sang In Lee, Sangsik Kim, Do Yoon Kim, and et al. 2025. "Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway" Antioxidants 14, no. 6: 694. https://doi.org/10.3390/antiox14060694

APA Style

Liu, Z., Huang, K., Huang, H., Kim, E., Kim, H., Kim, C. Y., Kim, D. J., Lee, S. I., Kim, S., Kim, D. Y., Liu, K., Ryoo, Z. Y., Lee, M.-H., Ma, L., & Kim, M. O. (2025). Isoquercitrin Suppresses Esophageal Squamous Cell Carcinoma (ESCC) by Inducing Excessive Autophagy and Promoting Apoptosis via the AKT/mTOR Signaling Pathway. Antioxidants, 14(6), 694. https://doi.org/10.3390/antiox14060694

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