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ONCOLOGY / BASIC RESEARCH
Anticancer activity of sulforaphane against human hepatoblastoma cells involves apoptosis, autophagy and inhibition of β-catenin signaling pathway
1
Department of Pediatric Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian Province, China
2
First Clinical Medical College, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian Province, China
Submission date: 2020-02-19
Final revision date: 2020-03-11
Acceptance date: 2020-03-22
Online publication date: 2020-06-04
Publication date: 2025-04-23
Corresponding author
Yali Xu
Department of Pediatric Surgery, The First Affiliated Hospital of Fujian, Medical University, 20 Chazhong Road, Fuzhou 350004, Fujian Province, China
Department of Pediatric Surgery, The First Affiliated Hospital of Fujian, Medical University, 20 Chazhong Road, Fuzhou 350004, Fujian Province, China
Arch Med Sci 2025;21(2):658-666
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Sulforaphane is an active isothiocyanate and has been reported to exhibit many pharmacological and biological activities including anticancer activity. The current study was undertaken to examine its anticancer activity against human hepatoblastoma.
Material and methods:
MTT and clonogenic assays were used to assess the antiproliferative effects of sulforaphane. Annexin V/PI staining and immunofluorescence microscopy were used to monitor the induction of apoptosis. GFP-LC3 transfection and fluorescence microscopy were used to investigate the induction of autophagy. Cell migration and invasion were assessed through wound healing and transwell chamber assay. Protein expression was determined by western blot analysis.
Results:
The results indicated that sulforaphane induced antiproliferative effects on the hepatoblastoma cell lines and exhibited an IC50 of 10 µM against the Hepu1 and HepU2 cells as compared to the IC50 of 90 µM against the normal THLE-2 cells. The antiproliferative effects were observed to be mediated via apoptosis which was accompanied by upregulation of Bax and suppression of Bcl-2 together with activation of caspase-3 and PARP cleavage. Sulforaphane also induced autophagy and the β-catenin signaling pathway. In addition, cell migration and cell invasion of the hepatoblastoma cells were also suppressed upon sulforaphane treatment.
Conclusions:
The results indicated that sulforaphane is a potential anticancer agent and may be considered as a lead molecule in the development of hepatoblastoma chemotherapy.
Sulforaphane is an active isothiocyanate and has been reported to exhibit many pharmacological and biological activities including anticancer activity. The current study was undertaken to examine its anticancer activity against human hepatoblastoma.
Material and methods:
MTT and clonogenic assays were used to assess the antiproliferative effects of sulforaphane. Annexin V/PI staining and immunofluorescence microscopy were used to monitor the induction of apoptosis. GFP-LC3 transfection and fluorescence microscopy were used to investigate the induction of autophagy. Cell migration and invasion were assessed through wound healing and transwell chamber assay. Protein expression was determined by western blot analysis.
Results:
The results indicated that sulforaphane induced antiproliferative effects on the hepatoblastoma cell lines and exhibited an IC50 of 10 µM against the Hepu1 and HepU2 cells as compared to the IC50 of 90 µM against the normal THLE-2 cells. The antiproliferative effects were observed to be mediated via apoptosis which was accompanied by upregulation of Bax and suppression of Bcl-2 together with activation of caspase-3 and PARP cleavage. Sulforaphane also induced autophagy and the β-catenin signaling pathway. In addition, cell migration and cell invasion of the hepatoblastoma cells were also suppressed upon sulforaphane treatment.
Conclusions:
The results indicated that sulforaphane is a potential anticancer agent and may be considered as a lead molecule in the development of hepatoblastoma chemotherapy.
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| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
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