AI Article Synopsis
- - SATB2 is a nuclear protein that plays a crucial role in gene regulation and stem cell properties, particularly in maintaining stemness and promoting epithelial-mesenchymal transition in various cell types, including prostate cancer cells.
- - The study finds that SATB2 is overexpressed in prostate cancer cell lines and cancer stem cells (CSCs), and inducing SATB2 expression in normal prostate epithelial cells leads to cancer-like properties such as colony formation and enhanced stem cell marker expression.
- - Knocking down SATB2 in prostate CSCs reduces their ability to form spheroids and colonies, while also affecting cell motility and migration, indicating that SATB2 is a key oncogenic factor in prostate cancer development and progression.
Article Abstract
Special AT-rich sequence binding protein-2 (SATB2) is a nuclear matrix protein that binds to nuclear attachment regions and is involved in chromatin remodeling and transcription regulation. In stem cells, it regulates the expression of genes required for maintaining pluripotency and self-renewal and epithelial-mesenchymal transition (EMT). In this study, we examined the oncogenic role of SATB2 in prostate cancer and assessed whether overexpression of SATB2 in human normal prostate epithelial cells (PrECs) induces properties of cancer stem cells (CSCs). The results demonstrate that SATB2 is highly expressed in prostate cancer cell lines and CSCs, but not in PrECs. Overexpression of SATB2 in PrECs induces cellular transformation which was evident by the formation of colonies in soft agar and spheroids in suspension. Overexpression of SATB2 in PrECs also resulted in induction of stem cell markers (CD44 and CD133), pluripotency-maintaining transcription factors (cMYC, OCT4, SOX2, KLF4, and NANOG), CADHERIN switch, and EMT-related transcription factors. Chromatin immunoprecipitation assay demonstrated that SATB2 can directly bind to promoters of BCL-2, BSP, NANOG, MYC, XIAP, KLF4, and HOXA2, suggesting SATB2 is capable of directly regulating pluripotency/self-renewal, cell survival, and proliferation. Since prostate CSCs play a crucial role in cancer initiation, progression, and metastasis, we also examined the effects of SATB2 knockdown on stemness. SATB2 knockdown in prostate CSCs inhibited spheroid formation, cell viability, colony formation, cell motility, migration, and invasion compared to their scrambled control groups. SATB2 knockdown in CSCs also upregulated the expression of E-CADHERIN and inhibited the expression of N-CADHERIN, SNAIL, SLUG, and ZEB1. The expression of SATB2 was significantly higher in prostate adenocarcinoma compared to normal tissues. Overall, our data suggest that SATB2 acts as an oncogenic factor where it is capable of inducing malignant changes in PrECs by inducing CSC characteristics.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11171950 | PMC |
| http://dx.doi.org/10.3390/cells13110962 | DOI Listing |
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