Triple-negative breast cancer (TNBC) lacks the protein expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). It is a special kind of breast cancer, accounting for 15 %− 25 % of all breast cancers [1]. TNBC has a strong ability of invasion and metastasis, with a high degree of malignancy. Most patients are in the late stage when diagnosed, and the recurrence rate is high, and the prognosis is poor [2], [4]. Compared with other subtypes of breast cancer, the effect of traditional endocrine therapy and targeted therapy is not effective because the hormone receptors of TNBC are negative. Moreover, once patients develop chemotherapy drug resistance, the tumor will rapidly relapse and metastasize, resulting in more severe disease [5]. Therefore, immunotherapy, new endocrine therapy and new targeted therapy have become the main research directions of TNBC, among which targeted therapy is the most promising direction to improve the survival of patients [6], [8].

Ubiquitin Carboxy-Terminal Hydrolase L1 (UCHL1) belongs to the ubiquitin carboxy-terminal hydrolase family, which is involved in the ubiquitin-mediated protein degradation pathway, and also has the functions of ubiquitin ligase and stabilizing intracellular ubiquitin monomer [9], [12]. Studies have shown that UCHL1 expression in TNBC is significantly higher than Luminal A, Luminal B and HER2+, and UCHL1 expression is related to the loss of ER expression [13]. Meanwhile, UCHL1 expression is negatively correlated with the prognosis of breast cancer and mediates multidrug resistance in breast cancer [14]. In addition, the majority of patients with ER+ breast cancer respond well to tamoxifen and fulvestrant at the beginning of treatment, but one-third of them with metastatic breast cancer later lose expression of ER and become resistant to hormonal therapy [15]. Therefore, UCHL1 may become a new and potential target for TNBC [14], [16], [17].

Cancer stem cells (CSCs) are tumor cells with the ability of self-renewal and infinite proliferation, and can produce heterogeneous tumor cells. It is characterized by unlimited self-renewal capacity, differentiation potential, high tumorigenicity and drug resistance [18], [20]. Studies have shown that cells with CD44+/CD24- phenotype in breast cancer have stem cell features in the aspects of self-renewal, proliferation and differentiation, which has become a hot spot in breast cancer research [21], [22]. In this paper, we detected the expression of UCHL1 in TNBC tissues and paired adjacent nontumor tissues by immunohistochemistry, and found that the protein level of UCHL1 in tumors was significantly higher than that in adjacent tissues, and was associated with poor prognosis. It was found that after overexpression of UCHL1 in TNBC cells, the number of CD44+/CD24- cells in TNBC cells increased, several CSC markers were upexpressed (CD44, NANOG, ABCG2, OCT4, SOX2) [23], [26], and the ability of spheroid formation was enhanced. Furthermore, UCHL1 may provide a good target for treating TNBC because it plays an important role in maintenance of tumor stemness in TNBC.