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Spalt-like transcription factor-2 (SALL2) suppresses breast carcinogenesis by inducing apoptosis and inhibiting cell migration and invasion
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DOI：10.3389/fgeed.2026.1788913.png)
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Abstract
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BackgroundSpalt-like transcription factor 2 (SALL2) has emerged as a potential tumor suppressor in various malignancies; however; its role in breast cancer remains underexplored. This study examines the effect of SALL2 overexpression on breast carcinogenesis; with a particular focus on the induction of apoptosis and inhibition of cell migration and invasion; using breast cancer receptor-positive and receptor-negative cell lines.MethodsBreast cancer cell lines (MCF-7 and MDA-MB-231) were transiently transfected with a SALL2 expression vector; and successful transfection was confirmed by real-time PCR and Western blot analysis. Functional assays performed included proliferation (MTT assay); wound healing; invasion (transwell Matrigel assay); apoptosis (flow cytometry); and assessment of mRNA expression levels of CDKN1A (p21); p16; PMAIP1 (NOXA); BAX; and MMP9 using quantitative real-time PCR.ResultsWe demonstrated that the transient upregulation of SALL2 expression markedly inhibited cell migration and invasion; processes central to tumor metastasis. This effect was accompanied by a reduction in MMP9; a key enzyme associated with extracellular matrix degradation and metastatic potential. Furthermore; upregulated SALL2 expression significantly promoted apoptosis; as evidenced by the upregulation of pro-apoptotic genes including PMAIP1 (NOXA); BAX; CDKN1A (p21); and p16. These changes suggest that SALL2 not only impedes metastatic capacity but also enhances apoptotic signaling pathways in breast cancer cells. Importantly; the tumor-suppressive nature of SALL2 was consistent in both types of breast cancer cell lines; underscoring its broad therapeutic relevance across different breast cancer subtypes.ConclusionOur findings indicate that SALL2 expression inhibits cell proliferation; migration; and invasion; while inducing apoptosis in breast cancer. These findings suggest that SALL2 may be a critical regulator of breast carcinogenesis and a potential target for therapeutics controlling tumor progression; invasion; and metastasis.
Keywords:
apoptosis
migration
breast cancer
invasion
spalt-like transcription factor
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