Sodium perborate tetrahydrate targets pancreatic cancer cells by inducing apoptosis, arresting the cell cycle, and disrupting cytoskeletal integrity.

BACKGROUND

Pancreatic cancer remains one of the most lethal malignancies worldwide due to its aggressive nature and resistance to conventional therapies. Novel agents that can simultaneously inhibit proliferation, induce apoptosis, and suppress metastasis are urgently needed. In this study, we investigated the anti-cancer potential of the boron-containing compound SPT in pancreatic cancer cell lines.

METHODS

The PSN-1 and BXPC-3 cell lines were treated with SPT at concentrations that corresponded to the half-maximal inhibitory concentration (IC50) value. The assessment of apoptosis was conducted through the utilisation of Annexin V/PI staining, in conjunction with the expression analysis of relevant apoptotic genes. Cell cycle distribution was analysed by flow cytometry, while quantitative PCR (qPCR) was used to evaluate the expression of key genes involved in the cell cycle, DNA damage response, and migration.

RESULT: SPT treatment induced a marked increase in apoptosis in both cell lines, which is demonstrated by the significant increase in both early and late apoptotic populations. The results of the study revealed that flow cytometry had revealed G0/G1 phase arrest in PSN-1 cells and G2/M arrest in BXPC-3 cells, which was associated with differential expression of CDKs, ATM, and ATR. Furthermore, SPT significantly inhibited DNA synthesis and colony formation. In addition, a number of genes associated with migration, including RhoA, Rac1, Cdc42, Vinculin and Tensin2, were found to be downregulated.

CONCLUSION

Sodium perborate tetrahydrate (SPT) emerges as a promising therapeutic compound, exhibiting selective cytotoxicity against pancreatic cancer cells by disrupting proliferation, cell cycle progression, and migratory potential.