BASIC RESEARCH
Allicin suppressed bladder cancer cell biological activities via regulation of the miR-26b-5p/PTEN axis in an in vitro study
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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
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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.