Study on the apoptosis of human melanoma cells induced by solanine in vitro and its mechanisms

Melanoma (malignant melanoma, MM) is a highly aggressive tumor, ranking as the third most common cutaneous malignancy and characterized by high metastatic potential, high mortality rates, and poor prognosis. Solanine, a major steroidal alkaloid found in potatoes, has widely reported anticancer benefits, though its inhibitory effects on melanoma cells are less studied. This study aimed to observe the effects of solanine on the proliferation, apoptosis, and related apoptotic proteins in melanoma A375 and A2058 cells and to investigate its possible anti-tumor mechanisms. The morphological changes associated with apoptosis induced by varying concentrations of solanine in melanoma cell lines A375 and A2058 were observed using an inverted microscope. The proliferation inhibition rate of melanoma cells was examined using the CCK-8 assay. DAPI staining was employed to observe cell growth and morphological changes. The apoptosis of melanoma A375 cells induced by solanine was detected using flow cytometry. The expression levels of apoptosis-related genes (Caspase-3, Bcl-2, and Bax) were measured using quantitative real-time PCR (RT-qPCR) and western blot analysis. Within a certain concentration and time range, solanine can inhibit the viability of A375 and A2058 cells significantly in a time-dose-dependent manner (P < 0.05). Apoptosis induced by solanine was confirmed through DAPI staining. Flow cytometry showed that, the proportion of Annexin V positive cells (the sum of early apoptotic cells and late apoptotic cells) increased gradually with the increasing of solanine dosage (P < 0.01). Notably, there was a marked decrease in the anti-apoptotic protein Bcl-2, alongside a significant increase in the expression of Bax and Caspase-3 at both the mRNA and protein levels (P < 0.05). Our data demonstrated that solanine inhibits the proliferation and induces apoptosis of melanoma A375 and A2058 cells. The findings indicate that these effects may be associated with the mitochondrial apoptotic pathway.