LAUSR

Triple-negative breast cancers (TNBCs) lack specific targeted therapy options and have evolved into highly chemoresistant tumors that metastasize to multiple organs. The present study demonstrated that the proline dehydrogenase (PRODH)mRNA level in paired (tumor vs. normal) human breast tissue samples (n1⁄4 234) was 6.6-fold greater than normal cells (*p1⁄4 0.021).We established stable PRODH-overexpressing TNBC (HS578T) cells, and themalignant phenotypeswere evaluated using soft agar colony formation andTranswellmigration assays. The results demonstrated that PRODH induced epithelial-mesenchymal transition in cancer cells and increased cell proliferation. The present study found that the tea polyphenol epigallocatechin-3-gallate (EGCG) significantly inhibited PRODH and its regulated proteins, such as alphasmooth muscle actin (alpha-SMA) expression in TNBC cells. These findings support the targeting of the PRODH signaling pathway as a potential therapeutic strategy in preventing cancer cellmetastasis. The patient-derived xenograft (PDX)mouse model is highly relevant to real human tumor growth.We established a TNBC-PDX (F4, n1⁄4 4 in each group) mousemodel. The PDXmice were treated with EGCG (50 mg/kg), and the results indicated that EGCG significantly inhibited PDX tumor growth (*p 1⁄4 0.013). These experiments provide additional evidence to evaluate the antitumor effects of EGCG-induced PRODH inhibition for clinical therapeutic application, especially in TNBC patients.