Post-treatment, we detected re-expression of tumour suppressor genes p53, p16, RASSF1A, RARb2, BRCA2, HIC1, ESR1, CDH1, TRbeta1, GSTP1 and CCND2 after inhibition of DNMT1mRNA. There was downregulation of metastatic ECM gene POEM (Arg-Gly-Asp) due to targeted scFv blocking binding to α8β1 integrin receptor with subsequent inhibition of adhesion, spreading and survival of metastatic tumour cells. There was inactivation of bcl-2,Raf-1 and cdc25c due to phosphorylation by vinorelbine. Furthermore, we detected upregulation of p21waf1, p27kip, Bid and Bak. The high energy radioisotopes induced DNA double-strand breaks in MBC cells and with MT depolymerizer agent vinorelbine they arrested their growth at the G2/M transition according to flow cytometry analysis. We detected externalization of PS, depolarization of mitochondrial transmembrane potential (ΔψM), activation of caspase-3, -7, -8 and -9 and bax, cleavage of poly(ADP-ribose)polymerase and DNA fragmentation. TEM exhibited irreversible D2 apoptotic signs, forming apoptotic bodies that were phagocytosed by adjacent tumor cells, leading to a bystander killing effect (BKE). BrdU and MTT exhibited inhibition of DNA synthesis and metabolic activity of treated MBC cells compared with untreated controls.