Activity of cyclin B1 in HL-60 cells treated with etoposide
Abstract
Cyclin B1 triggers G2/M phase transition phosphorylating with its catalytical partner - Cdc2 many of the molecular targets essential for cell cycle progression. Human leukemia cell line HL-60 were treated with increasing doses of etoposide (ETP) (0.5; 0.75; 1μM) to investigate how the drug affects cell morphology, viability, cell cycle distribution and expression of cyclin B1. To achieve this aim we applied light and transmission electron microscopy to observe morphological and ultra structural changes, image-based cytometry for apoptosis evaluation and cell cycle analysis, and then we conducted immunohistochemical and immunofluorescence staining to visualize cyclin localization and expression. Quantitive data about cyclin B1 expression were obtained from flow cytometry. Etoposide caused decrease in cell viability, induced apoptosis and G2/M arrest accompanied by enhanced expression of cyclin B1. Changes in expression and localization of cyclin B1 may constitute a part of the mechanism responsible for resistance of HL-60 cells to etoposide. Our results may reflect involvement of cyclin B1 in opposite processes - apoptosis induction and maintenance of cell viability in leukemia cells. We hypothesized possible roles and pathways by which cyclin B1 takes part in drug treatment response and chemosensitivity.
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This evidence supports multilevel regulation of the CDK1/cyclin B1 axis by MGF.
“This evidence supports multilevel regulation of the CDK1/cyclin B1 axis by MGF.”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [55]
In HL-60 cells, some studies reported increased CDK1 and cyclin B1 mRNA following MGF exposure, indicating regulation at the transcriptional level.
“In HL-60 cells, some studies have reported increased CDK1 and cyclin B1 mRNA following MGF exposure, indicating regulation at the transcriptional level in this model (55).”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [55]
Across tumor cell systems, the functional consequence of MGF exposure remains G2/M arrest, with reduced proliferation and increased susceptibility to apoptosis.
“However, across tumor cell systems, the functional consequence remains G2/M arrest, with reduced proliferation and increased susceptibility to apoptosis.”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [55]
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Mangiferin in human disease: Multifaceted mechanisms and applications (Review)
Dai, Y., Huang, Q., Tan, M., Wang, Z., Jiang, C., Liu, Z., Zhang, S., & Song, S. (2026) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2026.5736 · Cited by 3 · see citing works
“A comprehensive summary of the targets, dosages, study models, signaling pathways and mechanistic insights associated with MGF across different cancer‑related contexts is presented in Table I (4,5,7,8,13‑17,55,56,107‑114).”
- Authors
- Żuryń, A., Krajewski, A., Szulc, D., Litwiniec, A., & Grzanka, A.
- Affiliations
- Nicolaus Copernicus University (PL)
- Plant Breeding and Acclimatization Institute - National Research Institute (PL)
- Corresponding author
- Grzanka, Alina
- Venue
- Acta Histochemica
- Publisher
- Elsevier BV
- Published
- 2016-06
- Volume
- 118
- Issue
- 5
- Pages
- 537-543
- ISSN
- 0065-1281 (ISSN-L)
- OpenAlex
- W2439842789
- Cited by
- 12
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 1
- FWCI
- 0.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Acta Histochemica (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz (895)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- cyclin B1, etoposide, HL-60 cells, acute promyelocytic leukemia, apoptosis, G2/M cell cycle arrest, cdc2, drug resistance, cell viability, cell morphology, chemosensitivity
- MeSH terms
- Antineoplastic Agents, Phytogenic, Cell Division, Cell Survival, Etoposide, Humans, Apoptosis, HL-60 Cells, Drug Resistance, Neoplasm, Cyclin B1
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