Oncogenic mechanisms and therapeutic potential of SALL4 in hematological malignancies (Review)

As a member of the spalt like transcription factor (SALL) family, SALL4 regulates multiple oncogenic processes including cell proliferation, metastasis, epithelial-mesenchymal transition, cancer stem cell maintenance and drug resistance.Physiologically, it is essential for the self-renewal of embryonic and hematopoietic stem cells.Aberrant upregulation of SALL4 is frequently observed in both solid tumors and hematological malignancies; it has been proven to play a critical role in hematological malignancies, especially acute myeloid leukemia, acute lymphoblastic leukemia, myelodysplastic syndrome, chronic myeloid leukemia and mixed-lineage leukemia, where it promotes malignant cell proliferation, disease progression, and chemoresistance via downstream genes and key signaling pathways.Targeting key oncogenic molecules represents a promising therapeutic strategy for hematological malignancies.Elucidating the regulatory mechanisms of SALL4 may identify a novel therapeutic target.The present review summarizes the regulatory functions of SALL4 on key oncogenic targets and its upregulation profile in hematological malignancies.Although some mechanisms are mainly illustrated in solid tumors, they provide important insights for hematological cancer.Overall, SALL4 exhibits great potential as a novel therapeutic target and prognostic biomarker for hematological malignancies.Contents 1. Introduction 2. Downstream effects of SALL4 in tumors 3. Role of SALL4 in hematological malignancies 4. Challenges and future perspectives 5. Conclusions Oncogenic mechanisms and therapeutic potential of SALL4 in hematological malignancies (Review)