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ONCOLOGY / BASIC RESEARCH
Allicin suppressed bladder cancer cell biological activities via regulation of the miR-26b-5p/PTEN axis in an in vitro study
1
Department of Urology, First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, China
2
Department of Chinese Orthopedics and Traumatology, Second Hospital of Zhangjiakou City, Zhangjiakou, Hebei, China
3
Department of Drugs and Equipment, Second Hospital of Zhangjiakou City, Zhangjiakou, Hebei, China
Submission date: 2020-03-15
Final revision date: 2020-04-03
Acceptance date: 2020-04-04
Online publication date: 2020-05-03
Publication date: 2026-01-16
Corresponding author
Hongwei Su
Department of Urology First Affiliated Hospital of Hebei North University Zhangjiakou Hebei 075000, China
Department of Urology First Affiliated Hospital of Hebei North University Zhangjiakou Hebei 075000, China
Arch Med Sci 2025;21(6):2603-2627
KEYWORDS
TOPICS
ABSTRACT
Introduction:
The aim of this study was to investigate the anti-tumour effects of allicin in bladder cancer and to elucidate the related mechanisms by performing an in vitro study.
Material and methods:
Using the 5637 and T24 cell lines as model systems, the cell proliferation, apoptosis, cell invasion number and wound-healing rate were measured by MTT, flow cytometry, and Transwell and wound-healing assays. The expression of miR-26b-5p mRNA was evaluated by qRT-PCR assay, and relative protein expression (PTEN, PI3K and AKT) was evaluated by western blot assay. The correlation between miR-26b-5p and PTEN in 5637 and T24 cells was examined by the Dual Luciferase assay.
Results:
Compared with the normal control (NC) group, cell proliferation was significantly depressed as apoptosis increased (p < 0.05), the invasion cell number and wound-healing rate were significantly suppressed with allicin treatment, and miR-26b-5p was significantly down-regulated in a dose-dependent manner (p < 0.05); PTEN was significantly up-regulated, and PI3K and AKT proteins were significantly down-regulated (p < 0.05) in the allicin-treated groups. With miR-26b-5p transfection, the cell biological activities of 5367 and T24 were significantly restored compared with the allicin-treated group (p < 0.05), with PTEN significantly depressed and PI3K and AKT significantly increasing in 5637 and T24 cells (p < 0.05).
Conclusions:
Allicin has anti-tumour effects on bladder cancer cell biological activities, and the mechanism may involve regulation of the miR-26b-5p/PTEN axis in bladder cancer cells.
The aim of this study was to investigate the anti-tumour effects of allicin in bladder cancer and to elucidate the related mechanisms by performing an in vitro study.
Material and methods:
Using the 5637 and T24 cell lines as model systems, the cell proliferation, apoptosis, cell invasion number and wound-healing rate were measured by MTT, flow cytometry, and Transwell and wound-healing assays. The expression of miR-26b-5p mRNA was evaluated by qRT-PCR assay, and relative protein expression (PTEN, PI3K and AKT) was evaluated by western blot assay. The correlation between miR-26b-5p and PTEN in 5637 and T24 cells was examined by the Dual Luciferase assay.
Results:
Compared with the normal control (NC) group, cell proliferation was significantly depressed as apoptosis increased (p < 0.05), the invasion cell number and wound-healing rate were significantly suppressed with allicin treatment, and miR-26b-5p was significantly down-regulated in a dose-dependent manner (p < 0.05); PTEN was significantly up-regulated, and PI3K and AKT proteins were significantly down-regulated (p < 0.05) in the allicin-treated groups. With miR-26b-5p transfection, the cell biological activities of 5367 and T24 were significantly restored compared with the allicin-treated group (p < 0.05), with PTEN significantly depressed and PI3K and AKT significantly increasing in 5637 and T24 cells (p < 0.05).
Conclusions:
Allicin has anti-tumour effects on bladder cancer cell biological activities, and the mechanism may involve regulation of the miR-26b-5p/PTEN axis in bladder cancer cells.
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| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
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