【摘 要】
:
失巢凋亡指失去胞外贴附基质而引发的细胞死亡,实体肿瘤细胞耐受失巢凋亡是产生转移的生物学基础之一.细胞自噬是一种高度保守的依赖溶酶体降解受损大分子或细胞器的自我消化过程,从而循环利用降解产物.在实体肿瘤细胞转移过程中,细胞自噬起着不可或缺的作用.p66Shc是信号衔接蛋白ShcA的一个异构体,在正常表皮细胞中高表达,但在转移的非小细胞肺癌细胞中低表达或不表达,临床肺癌组织样品中其表达与患者存活时间负
【机 构】
:
天津医科大学基础医学院生物化学与分子生物学系 天津医学表观遗传学重点实验室;天津医学表观遗传学协同
【出 处】
:
第一届自噬生物学与疾病国际研讨会(The 1st International Symposium on Autophag
论文部分内容阅读
失巢凋亡指失去胞外贴附基质而引发的细胞死亡,实体肿瘤细胞耐受失巢凋亡是产生转移的生物学基础之一.细胞自噬是一种高度保守的依赖溶酶体降解受损大分子或细胞器的自我消化过程,从而循环利用降解产物.在实体肿瘤细胞转移过程中,细胞自噬起着不可或缺的作用.p66Shc是信号衔接蛋白ShcA的一个异构体,在正常表皮细胞中高表达,但在转移的非小细胞肺癌细胞中低表达或不表达,临床肺癌组织样品中其表达与患者存活时间负相关,淋巴细胞特异性转录因子Aiolos异位表达是抑制p66shc基因转录的原因,提示实体肿瘤细胞可能通过获得造血细胞的特性产生失巢凋亡抵抗,进而影响肿瘤的转移.当营养缺乏时,在肺癌A549细胞中用shRNA下调p66shc的表达,减缓了自噬过程、增强了失巢凋亡抵抗,提示p66shc调控细胞失巢凋亡和细胞自噬途径,因而调控p66Shc途径具有潜在的临床应用价值.
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