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SATB1 may reprogram energy metabolism in ovarian cancer by regulating lactate dehydrogenase and MCT1 levels to promote metastasis.
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Studies indicate Special AT-rich Sequence Binding Protein 1 (SATB1) to affect proliferation, cell cycle, apoptosis, cell morphology / cell polarity, EMT and multidrug-resistance as well as tumor formation, growth, invasion and metastasis [Review].
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Study results in bladder cancer are consistent with the conflicting data reported in other cancers, and that SATB1 might have different roles in cancer dependent on genetic background and stage of the cancer. The role of SATB1 is dependent on multiple factors, its use as a biomarker limited and as a therapeutic target likely highly variable among patients.
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The aim of this study was to investigate the expression of p16 and SATB1 proteins in regard to expression of the Ki-67 antigen and available clinicopathological data (i.a. receptor status, staging and grading
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HBx upregulated hepatic SATB1.
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Invasion and metastasis of GIN in Chinese patients correlates with SATB1 overexpression in tumor tissues, most profoundly in gastric cancer.
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High SATB1 expression is associated with Immunosuppressive Function of Regulatory T Cells in Chronic Hepatitis B.
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SATB2 can induce dedifferentiation by inducing stemness and may have a role in pancreatic carcinogenesis
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High SATB1 expression was associated with a better overall survival of patients with non-small cell lung carcinoma.ATB1 level correlates with Ki-67 expression in non-small cell lung carcinoma.
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These data implied that SATB1 might regulate gene expression through its different oligomerization state.
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High SATB1 expression is associated with glioblastoma.
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These findings suggest SATB1 may play an important role in OSCC invasiveness and metastasis.
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This paper provides evidence that SATB1 plays an oncogenic role in esophageal cancer by up-regulation of FN1 and PDGFRB.
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combination of the sequence-specific and nonspecific DNA-binding modes of SATB1 should be advantageous in a search for target loci during transcriptional regulation
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revealed more than 170 NFAT-associated proteins, half of which are involved in transcriptional regulation. Among them are many hitherto unknown interaction partners of NFATc1 and NFATc2 in T cells, such as Raptor, CHEK1, CREB1, RUNX1, SATB1, Ikaros, and Helios.
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SATB1 interacts directly with OGG1, increases its binding to 8-oxoG-containing DNA, promotes Schiff base formation, and stimulates its glycosylase and apyrimidinic/apurinic lyase enzymatic activities.
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High SATB1 expression in was detected in 48.3% of esophageal squamous cell carcinoma and 7.8% of normal esophagus tissues.
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Silencing of special AT-rich sequence binding protein 1 inhibited the proliferation of KYSE450 and EC9706 cells which have a relatively high level of special AT-rich sequence binding protein 1, and the ability of migration and invasion of KYSE450 and EC9706 cells was distinctly suppressed.
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Results suggest that SATB1 is activated to bind to chromatin at S/MARs after exposure to Abeta 1-42, resulting in alternative utilization and movement of 82-kDa ChAT to these regions demonstrating that both proteins play critical roles in the response of neural cells to acute Abeta-exposure.
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Our results highlight the significance of SATB1 in intrahepatic cholangiocarcinoma
