Objective: This study aimed to explore the molecular mechanisms of epithelial-mesenchymal transition (EMT) in breast cancer cells. Materials and Methods: GSE33146 microarray data downloaded from Gene Expression Omnibus (GEO). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of differentially expressed genes (DEGs) was performed, followed by functional annotation. Protein-protein interaction (PPI) network was constructed, and then five modules were mined for functional analysis. Results: A total of 507 DEGs including 229 up- and 278 down-regulated DEGs were screened between pre- and post-EMT samples. The screened DEGs mainly enriched in KEGG pathways, such as focal adhesion (p = 0.017), TGF-beta signaling pathway (p = 0.028), and ECM-receptor interaction (p = 6.89E-04), and also enriched in some GO terms such as regulation of cell proliferation (p = 2.48E-06) and ectoderm development (p = 2.76E-08). By functional analysis of DEGs, a total of ten proto-oncogenes including PBX1, MYBL1, MET, VAV3, and MYC, and 42 anti-oncogenes including TXNIP, TPM1, TMEFF2, TP63, and STEAP3 were obtained. Seven identified DEGs including SNCG, PTHLH, OAS1, KRT5, ITGB4, CHRM3, and CBLB were obtained. The constructed PPI network contained 192 nodes and 293 edges. A total of five models were screened from PPI network. DEGs in five modules were enriched in various functions, such as response to virus (FDR = 15.2), G-protein coupled receptor protein signaling pathway (FDR = 16.21), focal adhesion (FDR = 5.52E-05), and ECM-receptor interaction (FDR = 6.56E-07). Conclusions: The identified DEGs, especially in five modules, such as OAS1, IFI27, LPAR1, PTGFR, ITGB4, and ITGA6 might participate in EMT process for breast cancer cell lines DKTA.