Frontiers in genome editing · 2026
Spalt-like transcription factor-2 (SALL2) suppresses breast carcinogenesis by inducing apoptosis and inhibiting cell migration and invasion.
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Sisodiya Sandeep, Singh Payal, Gupta Suryanshi, Naugain Manvi, Rani Jyoti, Khan Asiya, Kumar Sandeep, Mishra Neetu, Tanwar Pranay, Hussain Showket
Аннотация
BACKGROUND: Spalt-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.
METHODS: Breast 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.
RESULTS: We 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.
CONCLUSION: Our 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.
METHODS: Breast 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.
RESULTS: We 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.
CONCLUSION: Our 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.