LEF1 (Lymphoid Enhancer-Binding Factor 1) is a transcription factor belonging to the High-Mobility Group (HMG) family of proteins, which plays a role in various biological processes, including cell proliferation, differentiation, and survival. LEF1 is a key downstream effector of the Wnt/β-catenin signaling pathway and can regulate the transcription of target genes by binding with β-catenin. In cancer research, the abnormal expression of LEF1 is associated with the occurrence and progression of various types of cancer. It also plays a role in stem cell maintenance and organ development, particularly in the process of Epithelial-Mesenchymal Transition (EMT), where it activates the transcription of EMT effectors such as N-Cadherin, Vimentin, and Snail. In certain cancer cell types, such as Chronic Lymphocytic Leukemia (CLL), Burkitt's Lymphoma (BL), Acute Lymphoblastic Leukemia (ALL), Oral Squamous Cell Carcinoma (OSCC), and Colorectal Cancer (CRC), the activity of LEF1 makes it a valuable biomarker for predicting patient prognosis. Furthermore, LEF1 promotes the expression and activity of the androgen receptor in prostate cancer in an androgen-independent manner, ultimately increasing the growth of prostate cancer regardless of androgen ablation therapy. LEF1's inhibition or knockdown has been shown to slow down cancer growth, migration, and invasion, making it a potential target for cancer treatment. In the context of hematological malignancies, the expression and function of LEF1 differ between normal and leukemic hematopoiesis, and its expression in Chronic Lymphocytic Leukemia (CLL) is closely related to the progression and prognosis of the disease. The upregulation of LEF1 in CLL/Small Lymphocytic Lymphoma (SLL) may begin at an early stage of the disease.
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