Abstract
Carcinogenesis is a long-drawn, multistep process, in which metastatic spread is an unequivocal hallmark of a poor prognosis. The progression and dissemination of epithelial cancers is commonly thought to rely on the epidermal-mesenchymal transition (EMT) process. During EMT, epithelial cells lose their junctions and apical-basal polarity, and they acquire a mesenchymal phenotype with its migratory and invasive capabilities. One of the proteins involved in cancer progression and EMT may be SATB1 (Special AT-Rich Binding Protein 1)—a chromatin organiser and a global transcriptional regulator. SATB1 organizes chromatin into spatial loops, providing a “docking site” necessary for the binding of further transcription factors and chromatin modifying enzymes. SATB1 has the ability to regulate whole sets of genes, even those located on distant chromosomes. SATB1 was found to be overexpressed in numerous malignancies, including lymphomas, breast, colorectal, prostate, liver, bladder and ovarian cancers. In the solid tumours, an elevated SATB1 level was observed to be associated with an aggressive phenotype, presence of lymph node, distant metastases, and a poor prognosis. In this review, we briefly describe the prognostic significance of SATB1 expression in most common human cancers, and analyse its impact on EMT and metastasis.
Highlights
Cancer is the second leading cause of death worldwide, accounting for more than 9 million deaths annually [1,2]
As we have shown in our recent study [91], Special AT-Rich Binding Protein 1 (SATB1) level was relatively high in the normal bronchial epithelium, whereas its expression was almost undetectable in the lung alveoli (Figure 2C,D, respectively)
SATB1 s expression was demonstrated to be positively correlated with the expression of Vimentin, and negatively with the expression of E-cadherin and CK20 [47]. These findings indicate that SATB1 may be an important factor influencing epidermal-mesenchymal transition (EMT) and metastasis in colorectal cancer (CRC) tumours
Summary
Cancer is the second leading cause of death worldwide, accounting for more than 9 million deaths annually [1,2]. SATB1 stimulated the expression of genes promoting metastasis, cell proliferation, angiogenesis and cell adhesion, whereas in the primary keratinocytes, it mainly regulated genes responsible for cell differentiation and development, as well as those coding keratin-associated proteins [31]. Its depletion had a reverse effect: an SATB1 knockdown in highly aggressive cancer cells was demonstrated to be enough to restore their normal morphology and decrease their migration and invasion abilities [17,49,50] These results could point to SATB1 s function as a specific trigger of a malignant phenotype, clearly contributing to carcinogenesis. We will consider the importance of SATB1 s expression in the progression of the five most common human neoplasms: cancers of the breast, lung, colorectum, prostate and stomach
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