DSBCl effectively reduced the expression of key biomarkers associated with tumor initiation, drug resistance, and metastatic potential, including CD24, ABCC2, and BCL2L1. Additionally, DSBCl downregulated genes related to tumorigenesis and pluripotency (NANOG, OCT4, and MYC) and induced the overexpression of the tumor suppressor genes KLF4 and KLF17, suggesting its potential to inhibit cell cycle progression and epithelial‒mesenchymal transition. This evidence concerns the gene KLF17 and neoplasm.