SATB2 linked to colon cancer stem cells

Scientists have identified a mechanism about how normal cells in the colon become malignant. Described online recently in Scientific Reports, their findings deepen our understanding of transformation and carcinogenesis and offer an attractive target for therapy, diagnosis, and prognosis of colon cancer.

Colon cancer, or colorectal cancer, is one of the leading causes of death worldwide, accounting for 655, 000 deaths per year globally. A growing body of evidence suggests that colorectal cancer stem cells are associated with transformation, progression, and metastasis. Cancer stem cells are a small population of cancer cells that have stem cell properties. Like normal stem cells, cancer stem cells have the capacity to self-renew and give rise to different cell types essential for tumor growth and survival. Cancer stem cells have been linked with treatment resistance, disease recurrence, and distant metastasis.

SATB2 (special AT-rich binding protein-2), a transcription factor, is known to regulate the expression of genes required for maintaining pluripotency and self-renewal. SATB2 is assumed to be a regulator of malignant transformation of human colorectal epithelial cells. But the molecular mechanisms in this process remain unknown.

To solve this mystery, researchers headed by Rakesh Srivastava from Kansas City VA Medical Center conducted this study. First, they measured SATB2 expression in human normal colon epithelial cells and several human colorectal cancer cell lines. They did not detect SATB2 in human normal colon epithelial cells but observed relatively high levels of SATB2 in all colorectal cancer cell lines studied.

To verify the role of SATB2 in cell transformation and stemness, the researchers overexpressed SATB2 in human normal colon epithelial cells. Overexpression of SATB2 led to the expression of stem cell-associated molecules as well as increased cell growth, migration, and invasion. The results prove that SATB2 is able to induce malignant transformation of human normal colon epithelial cells.

Next, they inhibited SATB2 in colorectal cancer stem cells. The results showed that inhibition of SATB2 suppressed the expression of stem cell markers and led to reduced cell migration and invasion. Furthermore, they identified the β-catenin/TCF-LEF pathway as a mediator of the biological effects of SATB2.

In summary, the study proves that SATB2 is able to induce malignant transformation in normal colorectal epithelial cells, and that SATB2 overexpression is crucial for the maintaining of cancer stem cells, whereas SATB2 inhibition eliminates cancer stem cell properties. Because SATB2 is differentially expressed between normal and cancer colon cells, drugs that target SATB2 might kill colon cancer cells, sparing normal cells.
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