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Updated: Feb 23, 2026
Author Spotlight: Assessing the Potential of Circulating Tumor Cells in Leptomeningeal Disease Research
Published on: March 29, 2024
Antitumor activity and expression profiles of genes induced by sulforaphane in human melanoma cells
Paola Arcidiacono1,2, Francesco Ragonese1, Anna Stabile3
1Department of Life Sciences, Imperial College London, London SW7 2AZ, United KingdomDepartment of Experimental Medicine, University of Perugia, Piazza Lucio Severi, 06132, Perugia, Italy.
Purpose:
Human melanoma is a highly aggressive incurable cancer due to intrinsic cellular resistance to apoptosis, reprogramming, proliferation and survival during tumour progression. Sulforaphane (SFN), an isothiocyanate found in cruciferous vegetables, plays a role in carcinogenesis in many cancer types. However, the cytotoxic molecular mechanisms and gene expression profiles promoted by SFN in human melanoma remain unknown.
Methods:
Three different cell lines were used: two human melanoma A375 and 501MEL and human epidermal melanocytes (HEMa). Cell viability and proliferation, cell cycle analysis, cell migration and invasion and protein expression and phosphorylation status of Akt and p53 upon SFN treatment were determined. RNA-seq of A375 was performed at different time points after SFN treatment.
Results:
We demonstrated that SFN strongly decreased cell viability and proliferation, induced G2/M cell cycle arrest, promoted apoptosis through the activation of caspases 3, 8, 9 and hampered migration and invasion abilities in the melanoma cell lines. Remarkably, HEMa cells were not affected by SFN treatment. Transcriptomic analysis revealed regulation of genes involved in response to stress, apoptosis/cell death and metabolic processes. SFN upregulated the expression of pro-apoptotic genes, such as p53, BAX, PUMA, FAS and MDM2; promoted cell cycle inhibition and growth arrest by upregulating EGR1, GADD45B, ATF3 and CDKN1A; and simultaneously acted as a potent inhibitor of genotoxicity by launching the stress-inducible protein network (HMOX1, HSPA1A, HSPA6, SOD1).
Conclusion:
Overall, the data show that SFN cytotoxicity in melanoma derives from complex and concurrent mechanisms during carcinogenesis, which makes it a promising cancer prevention agent.
Insights
Sulforaphane (SFN) effectively reduced melanoma cell viability and proliferation, inducing apoptosis and cell cycle arrest. This natural compound shows promise as a cancer prevention agent by targeting complex mechanisms in melanoma progression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Human melanoma is an aggressive cancer characterized by resistance to apoptosis, proliferation, and survival mechanisms.
- Sulforaphane (SFN), a compound from cruciferous vegetables, has shown roles in various cancer types, but its specific cytotoxic mechanisms in melanoma are not fully understood.
Purpose of the Study:
- To investigate the molecular mechanisms and gene expression profiles induced by SFN in human melanoma cells.
- To determine the effects of SFN on melanoma cell viability, proliferation, cell cycle, migration, invasion, and apoptosis.
Main Methods:
- Utilized human melanoma cell lines (A375, 501MEL) and normal human epidermal melanocytes (HEMa).
- Assessed cell viability, proliferation, cell cycle, migration, and invasion.
- Analyzed protein expression and phosphorylation of Akt and p53.
- Performed RNA sequencing (RNA-seq) on A375 cells treated with SFN.
Main Results:
- SFN significantly decreased melanoma cell viability and proliferation, inducing G2/M cell cycle arrest and apoptosis via caspase activation.
- SFN inhibited melanoma cell migration and invasion, while normal melanocytes remained unaffected.
- Transcriptomic analysis revealed SFN modulates genes involved in stress response, apoptosis, and metabolism, upregulating pro-apoptotic genes (e.g., p53, BAX) and cell cycle inhibitors (e.g., EGR1, CDKN1A), while also inhibiting genotoxicity via stress-inducible proteins (e.g., HMOX1, SOD1).
Conclusions:
- SFN exhibits potent cytotoxicity in melanoma through multifaceted and concurrent mechanisms.
- These findings highlight SFN's potential as a promising agent for cancer prevention in melanoma.
