Epigenetic Silencing of TAP1 in Aldefluor+ Breast Cancer Stem Cells Contributes to Their Enhanced Immune Evasion.
作者： Mohammad Sultan , Dejan Vidovic , Arianne S. Paine , Thomas T. Huynh , Krysta M. Coyle
DOI: 10.1002/STEM.2780
关键词:
摘要: Avoiding detection and destruction by immune cells is key for tumor initiation progression. The important role of cancer stem (CSCs) in has been well established, yet their ability to evade targeting only partly understood. To investigate the breast CSCs detection, we identified a highly tumorigenic population spontaneous murine mammary based on increased aldehyde dehydrogenase activity. We performed growth studies immunocompetent immunocompromised mice. In mice, was restricted; however, Aldefluor+ expanded, suggesting inherent resistance mechanisms. Gene expression analysis sorted revealed that decreased transporter associated with antigen processing (TAP) genes co-stimulatory molecule CD80, which would decrease susceptibility T cells. Similarly, patient tumors 4T1 had TAP genes. contrast, CD44+ CD24- do not have these genes, but C-X-C chemokine receptor type 4. Decitabine treatment bisulfite pyrosequencing suggests DNA hypermethylation contributes gene CSCs. TAP1 knockdown resulted Together, this evasion mechanisms are marker specific epigenetic silencing enhanced survival under pressure. Stem Cells 2018;36:641-654.
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