High expression of FUSE binding protein 1 in breast cancer stimulates cell proliferation and diminishes drug sensitivity.

Breast cancer is the most common malignant tumor affecting women worldwide and is divided into the following subtypes: Luminal A, Luminal B, HER‑2 overexpression and triple‑negative breast cancer (TNBC). TNBC accounts for approximately 15‑20% of all breast cancer cases. Due to the characteristics of low differentiation, the likelyhood of recurrence and metastasis, strong invasiveness and the lack of hormone receptors and human epidermal growth factor receptor 2 (HER2), patients with TNBC cannot benefit from endocrine therapy or other available targeted agents. Chemotherapy is one of the main treatments for patients with TNBC, and cisplatin is one of the most commonly used and effective drugs. The human far upstream element binding protein 1 (FBP1) is a potent pro‑proliferative and anti‑apoptotic oncoprotein, which is overexpressed in numerous tumor types. The present study demonstrated that FBP1 and its target, c‑Myc, were more highly expressed in breast cancer tissues compared with para‑carcinoma tissues, and the FBP1 and c‑Myc levels are decreased by cisplatin treatment. The knockdown of FBP1 in TNBC cells decreased cell proliferation by arresting the cell cycle at the G2 phase. The knockdown of FBP1 decreased the expression of G2 phase‑associateed protein cyclin A2, whereas it increased that of cyclin B1 and p‑CDC2. Furthermore, the knockdown of FBP1 decreased cell migration and metastasis by downregulating matrix metalloproteinase 2 expression, and enhanced the sensitivity of TNBC cells to cisplatin by inducing apoptosis. These results thus suggest that FBP1 is a potential novel biological marker for the diagnosis and treatment of TNBC.