高表达 CD133 的癌细胞可上调 FLIP 的表达，从而抵抗 TRAIL 诱导的细胞凋亡。
Cancer cells with high expression of CD133 exert FLIP upregulation and resistance to TRAIL-induced apoptosis.
机构信息
Apoptosis Research Group, School of Medical Science, Griffith University, Southport, Qld, Australia.
出版信息
Biofactors. 2008;34(3):231-5. doi: 10.3233/BIO-2009-1076.
It is increasingly accepted that cancer stem cells (CSCs) are rather resistant to apoptosis to various inducers, including the immunological apoptogen TRAIL. Here we show that cancer cells with high expression of CD133, a marker that is often associated with CSCs, are resistant to TRAIL-induced apoptosis, compared to their CD133-low counterparts. We show that this resistance can be ascribed to the high expression of FLIP, an inhibitor of the extrinsic apoptotic pathway, in CD133-high cells. Downregulation of FLIP by siRNA in CD133-high cells sensitised them to TRAIL killing. Thus, CD133-high cells may be resistant to TRAIL due to high expression of FLIP.
越来越多的人认为，癌症干细胞（CSC）对各种诱导剂（包括免疫凋亡原 TRAIL）的凋亡具有很强的抵抗力。在这里，我们发现，与 CD133 低表达的细胞相比，高表达 CD133 的细胞（该标志物通常与 CSC 相关）对 TRAIL 诱导的凋亡具有抗性。我们发现，这种抗性可以归因于 CD133 高表达细胞中抑制外在凋亡途径的 FLIP 的高表达。用 siRNA 下调 CD133 高表达细胞中的 FLIP 可使它们对 TRAIL 杀伤敏感。因此，CD133 高表达细胞可能由于 FLIP 的高表达而对 TRAIL 产生抗性。
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