A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathway

Introduction: Globally, colorectal cancer (CRC) is the third most common type of cancer, and its treatment frequently includes the utilization of drugs based on antibodies and small molecules. The development of CRC has been linked to various signaling pathways, with the Wnt/β-catenin pathway identi...

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Main Authors: Min Hee Yang, Basappa Basappa, Suresha N. Deveshegowda, Akshay Ravish, Arunkumar Mohan, Omantheswara Nagaraja, Mahendra Madegowda, Kanchugarakoppal S. Rangappa, Amudha Deivasigamani, Vijay Pandey, Peter E. Lobie, Kam Man Hui, Gautam Sethi, Kwang Seok Ahn
Format: Article
Language:English
Published: Elsevier 2025-06-01
Series:Journal of Advanced Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S2090123224003059
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author Min Hee Yang
Basappa Basappa
Suresha N. Deveshegowda
Akshay Ravish
Arunkumar Mohan
Omantheswara Nagaraja
Mahendra Madegowda
Kanchugarakoppal S. Rangappa
Amudha Deivasigamani
Vijay Pandey
Peter E. Lobie
Kam Man Hui
Gautam Sethi
Kwang Seok Ahn
author_facet Min Hee Yang
Basappa Basappa
Suresha N. Deveshegowda
Akshay Ravish
Arunkumar Mohan
Omantheswara Nagaraja
Mahendra Madegowda
Kanchugarakoppal S. Rangappa
Amudha Deivasigamani
Vijay Pandey
Peter E. Lobie
Kam Man Hui
Gautam Sethi
Kwang Seok Ahn
author_sort Min Hee Yang
collection DOAJ
description Introduction: Globally, colorectal cancer (CRC) is the third most common type of cancer, and its treatment frequently includes the utilization of drugs based on antibodies and small molecules. The development of CRC has been linked to various signaling pathways, with the Wnt/β-catenin pathway identified as a key target for intervention. Objectives: We have explored the impact of imidazopyridine-tethered chalcone-C (CHL-C) in CRC models. Methods: To determine the influence of CHL-C on apoptosis and autophagy, Western blot analysis, annexin V assay, cell cycle analysis, acridine orange staining, and immunocytochemistry were performed. Next, the activation of the Wnt/β-catenin signaling pathway and the anti-cancer effects of CHL-C in vivo were examined in an orthotopic HCT-116 mouse model. Results: We describe the synthesis and biological assessment of the CHL series as inhibitors of the viability of HCT-116, SW480, HT-29, HCT-15, and SNU-C2A CRC cell lines. Further biological evaluations showed that CHL-C induced apoptosis and autophagy in down-regulated β-catenin, Wnt3a, FZD-1, Axin-1, and p-GSK-3β (Ser9), and up-regulated p-GSK3β (Tyr216) and β-TrCP. In-depth analysis using structure-based bioinformatics showed that CHL-C strongly binds to β-catenin, with a binding affinity comparable to that of ICG-001, a well-known β-catenin inhibitor. Additionally, our in vivo research showed that CHL-C markedly inhibited tumor growth and triggered the activation of both apoptosis and autophagy in tumor tissues. Conclusion: CHL-C is capable of inducing apoptosis and autophagy by influencing the Wnt/β-catenin signaling pathway.
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spelling doaj-art-a96c1a5683024c83bb50f11096d643322025-08-20T03:47:41ZengElsevierJournal of Advanced Research2090-12322025-06-017261563210.1016/j.jare.2024.07.022A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathwayMin Hee Yang0Basappa Basappa1Suresha N. Deveshegowda2Akshay Ravish3Arunkumar Mohan4Omantheswara Nagaraja5Mahendra Madegowda6Kanchugarakoppal S. Rangappa7Amudha Deivasigamani8Vijay Pandey9Peter E. Lobie10Kam Man Hui11Gautam Sethi12Kwang Seok Ahn13Department of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Republic of KoreaLaboratory of Chemical Biology, Department of Studies in Organic Chemistry, University of Mysore, Manasagangotri, Mysore 570006, IndiaLaboratory of Chemical Biology, Department of Studies in Organic Chemistry, University of Mysore, Manasagangotri, Mysore 570006, IndiaLaboratory of Chemical Biology, Department of Studies in Organic Chemistry, University of Mysore, Manasagangotri, Mysore 570006, IndiaLaboratory of Chemical Biology, Department of Studies in Organic Chemistry, University of Mysore, Manasagangotri, Mysore 570006, IndiaDepartment of Studies in Physics, University of Mysore, Manasagangotri, Mysore 570006, IndiaDepartment of Studies in Physics, University of Mysore, Manasagangotri, Mysore 570006, IndiaLaboratory of Chemical Biology, Department of Studies in Organic Chemistry, University of Mysore, Manasagangotri, Mysore 570006, IndiaDivision of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre Singapore, 169610, SingaporeShenzhen Bay Laboratory, Shenzhen 518055, China; Tsinghua Berkeley Shenzhen Institute, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China; Institute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, ChinaShenzhen Bay Laboratory, Shenzhen 518055, China; Tsinghua Berkeley Shenzhen Institute, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, China; Institute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen 518055, ChinaDivision of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre Singapore, 169610, Singapore; Corresponding author at: Division of Cellular and Molecular Research, Humphrey Oei Institute of Cancer Research, National Cancer Centre Singapore, 169610, Singapore.Department of Pharmacology and NUS Centre for Cancer Research (N2CR), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore; Corresponding author at: Department of Pharmacology and NUS Centre for Cancer Research (N2CR), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore.Department of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea; Corresponding author at: Department of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.Introduction: Globally, colorectal cancer (CRC) is the third most common type of cancer, and its treatment frequently includes the utilization of drugs based on antibodies and small molecules. The development of CRC has been linked to various signaling pathways, with the Wnt/β-catenin pathway identified as a key target for intervention. Objectives: We have explored the impact of imidazopyridine-tethered chalcone-C (CHL-C) in CRC models. Methods: To determine the influence of CHL-C on apoptosis and autophagy, Western blot analysis, annexin V assay, cell cycle analysis, acridine orange staining, and immunocytochemistry were performed. Next, the activation of the Wnt/β-catenin signaling pathway and the anti-cancer effects of CHL-C in vivo were examined in an orthotopic HCT-116 mouse model. Results: We describe the synthesis and biological assessment of the CHL series as inhibitors of the viability of HCT-116, SW480, HT-29, HCT-15, and SNU-C2A CRC cell lines. Further biological evaluations showed that CHL-C induced apoptosis and autophagy in down-regulated β-catenin, Wnt3a, FZD-1, Axin-1, and p-GSK-3β (Ser9), and up-regulated p-GSK3β (Tyr216) and β-TrCP. In-depth analysis using structure-based bioinformatics showed that CHL-C strongly binds to β-catenin, with a binding affinity comparable to that of ICG-001, a well-known β-catenin inhibitor. Additionally, our in vivo research showed that CHL-C markedly inhibited tumor growth and triggered the activation of both apoptosis and autophagy in tumor tissues. Conclusion: CHL-C is capable of inducing apoptosis and autophagy by influencing the Wnt/β-catenin signaling pathway.http://www.sciencedirect.com/science/article/pii/S2090123224003059CHL-CWnt/ β −cateninApoptosisAutophagyColorectal cancer
spellingShingle Min Hee Yang
Basappa Basappa
Suresha N. Deveshegowda
Akshay Ravish
Arunkumar Mohan
Omantheswara Nagaraja
Mahendra Madegowda
Kanchugarakoppal S. Rangappa
Amudha Deivasigamani
Vijay Pandey
Peter E. Lobie
Kam Man Hui
Gautam Sethi
Kwang Seok Ahn
A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathway
Journal of Advanced Research
CHL-C
Wnt/ β −catenin
Apoptosis
Autophagy
Colorectal cancer
title A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathway
title_full A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathway
title_fullStr A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathway
title_full_unstemmed A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathway
title_short A novel drug prejudice scaffold-imidazopyridine-conjugate can promote cell death in a colorectal cancer model by binding to β-catenin and suppressing the Wnt signaling pathway
title_sort novel drug prejudice scaffold imidazopyridine conjugate can promote cell death in a colorectal cancer model by binding to β catenin and suppressing the wnt signaling pathway
topic CHL-C
Wnt/ β −catenin
Apoptosis
Autophagy
Colorectal cancer
url http://www.sciencedirect.com/science/article/pii/S2090123224003059
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