Spalt-like transcription factor-2 (SALL2) suppresses breast carcinogenesis by inducing apoptosis and inhibiting cell migration and invasion
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Sandeep Sisodiya1,2, Payal Singh1,3, Suryanshi Gupta1,4
1Cellular and Molecular Diagnostics (Molecular Biology Group), National Institute of Cancer Prevention and Research (ICMR), Noida, India.
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.
Insights
Spalt-like transcription factor 2 (SALL2) suppresses breast cancer progression by inhibiting cell migration and invasion. Overexpression of SALL2 also promotes apoptosis, suggesting its therapeutic potential against breast cancer metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Spalt-like transcription factor 2 (SALL2) is a potential tumor suppressor with an under-explored role in breast cancer.
- This study investigates the impact of SALL2 on breast carcinogenesis, focusing on apoptosis, cell migration, and invasion.
Purpose of the Study:
- To examine the effect of SALL2 overexpression on breast cancer cell lines.
- To determine SALL2's influence on apoptosis, cell migration, and invasion.
- To assess SALL2's potential as a therapeutic target in breast cancer.
Main Methods:
- Transient transfection of breast cancer cell lines (MCF-7, MDA-MB-231) with a SALL2 expression vector.
- Confirmation of SALL2 upregulation via real-time PCR and Western blot.
- Functional assays including proliferation, wound healing, invasion, apoptosis, and gene expression analysis (p21, p16, NOXA, BAX, MMP9).
Main Results:
- SALL2 overexpression significantly inhibited cell migration and invasion, correlating with decreased MMP9 levels.
- Upregulated SALL2 promoted apoptosis through increased expression of pro-apoptotic genes (NOXA, BAX, p21, p16).
- SALL2 demonstrated tumor-suppressive effects consistently across receptor-positive and receptor-negative breast cancer cell lines.
Conclusions:
- SALL2 inhibits breast cancer cell proliferation, migration, and invasion while inducing apoptosis.
- SALL2 acts as a critical regulator in breast carcinogenesis.
- SALL2 represents a potential therapeutic target for controlling breast cancer progression, invasion, and metastasis.
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