Dihydrotanshinone I promotes apoptosis and inhibits proliferation in SH-SY5Y neuroblastoma cells
Year: 2026
Type: article
Abstract: Introduction Dihydrotanshinone I is known to exhibit antineoplastic properties. However, its effects on neuroblastoma, a common pediatric malignancy, remain unexplored. This in vitro study investigated the effects of dihydrotanshinone I in SH-SY5Y neuroblastoma cells using proliferation, viability, apoptosis, and transcriptomic assays. Methods The effects of dihydrotanshinone I were investigated through treatment of SH-SY5Y neuroblastoma cells with graded concentrations. Cell proliferation was assessed based on the EdU incorporation test alongside cell counting. Cell viability/cytotoxicity were detected via Calcein/propidium iodide staining. Cell apoptosis was measured by Caspase-3 activity assays and Annexin V staining. To elucidate the possible mechanism involved for dihydrotanshinone I, transcriptome sequencing was performed for comprehensive investigation of the changes in gene expression, and then differential expression functional enrichment analysis was performed. Results Dihydrotanshinone I suppressed cell proliferation in a dose-dependent fashion, accompanied by morphological changes, cell detachment, and cell death. Total cell counts declined, with greater dead cell percentages at higher concentrations. EdU-positive cells were diminished, suggesting inhibition of proliferation. Morphological signs of apoptosis were apparent. Transcriptomic analysis indicated enrichment of the p53 signaling pathway among DHT-modulated genes, and Western blot analysis further confirmed activation of this pathway at the protein level. Conclusion DHT reduced SH-SY5Y proliferation in a dose-dependent manner and increased apoptotic cell death, with transcriptomic and Western blot data implicating the p53 signaling pathway, suggesting that it warrants further investigation as a potential anti-neuroblastoma candidate.
Language: English
Subfield: Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $1,400
Funders: National Natural Science Foundation of China, Chongqing Medical University, Natural Science Foundation of Beijing Municipality, Peking University, National University's Basic Research Foundation of China, Capital Health Research and Development of Special Fund, National Key Research and Development Program of China, Fundamental Research Funds for the Central Universities
OpenAlex ID: W7204469756