Abstract
Triple‑negative breast cancer (TNBC) is a type of breast cancer that is characterized by the lack of expression of estrogen and progesterone receptors, and epidermal growth factor receptor 2. Therefore, there is an absence of a specific target for effective therapy in TNBC. Cisplatin is usually employed as a first‑line chemotherapy agent for patients with TNBC. However, resistance remains an obstacle for cisplatin‑based chemotherapy, due to its elusive underlying mechanism. Previously, abnormal expression of Islet 1 (ISL1) was demonstrated to be closely associated with cancer development and progression. The present study revealed that (ISL1) was significantly upregulated in TNBC tissues in comparison with adjacent normal tissues. Overexpression of ISL1 markedly promoted the proliferation and invasion of the TNBC MDA‑MB‑231 and MDA‑MB‑468 cell lines, while knockdown of ISL1 inhibited cell invasion and proliferation in these cell lines. In addition, overexpression of ISL1 reversed cisplatin‑induced cell apoptosis, while knockdown of ISL1 enhanced apoptosis following cisplatin treatment in MDA‑MB‑231 and MDA‑MB‑468 cells. Furthermore, the levels of the anti‑apoptotic proteins, phosphorylated‑protein kinase B and B‑cell lymphoma‑2 (Bcl‑2), were significantly decreased, while the levels of the pro‑apoptotic protein Bcl‑2‑associated X protein were remarkably increased in response to cisplatin treatment. The present study revealed that ISL1 overexpression reversed the protein expression profile of p‑Akt, Bcl‑2 and Bax, while ISL1 knockdown promoted cell apoptosis. Therefore, the data of the present study demonstrated that ISL1 contributes to TNBC progression and reverses cell sensitivity towards cisplatin in TNBC cells, suggesting that ISL1 is a potential therapeutic target for the treatment of TNBC.