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Cited by 62Flavonoids in Medical ResearchPhytochemicals and Antioxidant ActivitiesCell death mechanisms and regulation

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Quercetin-Mediated Apoptosis and Cellular Senescence in Human Colon Cancer

Özsoy, Serpil, Becer, Eda, Kabadayı, Hilal, Vatansever, Hafize S., Yücecan, Sevinç·2020·Anti-Cancer Agents in Medicinal Chemistry
DOI 10.2174/1871520620666200408082026
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Abstract

Background: Quercetin is a flavonol from the flavonoid group of polyphenols, which positively affects human health due to its anti-cancer, anti-inflammatory, anti-microbial and cardioprotective effects. The effects of phenolic compounds, including quercetin, on programmed cell death and cellular senescence, have been the subject of research in recent years. Objective: In this study, we aimed to investigate the effects of quercetin on cell viability, apoptosis and cellular senescence in primary (Colo-320) and metastatic (Colo-741) colon adenocarcinoma cell lines. Methods: Cytotoxicity was analyzed via MTT assay in Colo-320 and Colo-741 cell lines. After quercetin treatment, cell ularsenescence and apoptosis were evaluated by TUNEL staining, X-Gal staining and indirect peroxidase technique for immunocytochemical analysis of related proteins such as Bax, Bcl-2, caspase-3, Hsp27, Lamin B1, p16, cyclin B1. Results: The effective dose for inhibition of cell growth in both cell lines was determined to be 25μg/ml quercetin for 48 hours. Increased Baximmunoreactivityfollowingquercetin treatment was significant in both Colo-320 and Colo-741 cell lines, but decreased Bcl-2 immunoreactivitywas significant only in theColo-320 primary cell line. In addition, after quercetin administration, the number of TUNEL positive cells and, immunoreactivities for p16, Lamin B1 and cyclin B1 in both Colo-320 and Colo-741 cells increased. Conclusion: Our results suggest that quercetin may only induce apoptosis in primary colon cancer cells. Furthermore, quercetin also triggered senescence in colon cancer cells, but some cells remained alive, suggesting that colon cancer cells might have escaped from senescence.

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Metadata

Authors
Özsoy, S., Becer, E., Kabadayı, H., Vatansever, H. S., & Yücecan, S.
Affiliations
  • Near East University (CY)
  • Manisa Celal Bayar University (TR)
  • DESAM Institute, Near East University, Nicosia, Cyprus
Corresponding author
Özsoy, Serpil
ORCID
Venue
Anti-Cancer Agents in Medicinal Chemistry
Publisher
Bentham Science Publishers Ltd.
Published
2020-07-08
Volume
20
Issue
11
Pages
1387-1396
ISSN
  • 1568-0118 (ISSN-L)
  • 1871-5206
DOI
10.2174/1871520620666200408082026
OpenAlex
W3015500267
Cited by
62
References
33
Citations by year
2026: 3 · 2025: 9 · 2024: 11 · 2023: 13 · 2022: 14 · 2021: 10 · 2020: 2
FWCI
5.85
Type
journal article
Language
en
Open access
closed
Locations
  • Anti-Cancer Agents in Medicinal Chemistry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pharmacology (medical) › Flavonoids in Medical Research
  • Health Sciences › Medicine › Biochemistry (medical) › Phytochemicals and Antioxidant Activities
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
quercetin, apoptosis, cellular senescence, colon cancer, colon adenocarcinoma, flavonoids, polyphenols, Bax, Bcl-2, p16, lamin B1, cyclin B1, caspase-3, HSP27, metastatic colon cancer, cytotoxicity
MeSH terms
Antineoplastic Agents, Cell Survival, Cells, Cultured, Colonic Neoplasms, Dose-Response Relationship, Drug, Drug Screening Assays, Antitumor, Humans, Quercetin, Structure-Activity Relationship, Molecular Structure, Cellular Senescence, Apoptosis, Cell Proliferation

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CoChat. (2026). Citation check: Quercetin-Mediated Apoptosis and Cellular Senescence in Human Colon Cancer. https://app.cochat.ai/papers/10.2174/1871520620666200408082026
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Özsoy, S., Becer, E., Kabadayı, H., Vatansever, H. S., & Yücecan, S. (2020). Quercetin-Mediated Apoptosis and Cellular Senescence in Human Colon Cancer. Anti-Cancer Agents in Medicinal Chemistry. https://doi.org/10.2174/1871520620666200408082026