摘要
食管腺癌(EAC)是世界上增长最快的癌症之一。它的发生主要是由于慢性胃食管反流病(GERD),在此期间食管上皮经常暴露于从胃上来的酸性液体。这引发食管细胞的基因突变,可能导致EAC的发展。当p53被激活以清除突变细胞时,NF -κB协调剩余的细胞来愈合伤口。然而,如果突变发生在TP53(一种常见情况),突变产物转而支持肿瘤发生。在这种情况下,NF -κB与突变体p53一起促进癌症进展。TRAIL是GERD发作产生的一种细胞因子,它可以选择性地杀死癌细胞,但临床应用并不像预期的那样成功,因为一些高度复杂的防御机制已经在恶性肿瘤中发展起来。为了清除后续行动的障碍,需要使用第二种药剂来解除癌细胞的武装。CCN1似乎就是这样一种分子。CCN1在支持正常食管细胞生长的同时,通过抑制NFκB抑制恶性转化,并通过TRAIL诱导凋亡杀死EAC细胞。
关键词: 食管癌,p53
图形摘要
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