Differential senescence capacities in meibomian gland carcinoma andbasal cell carcinoma.
Differential senescence capacities in meibomian gland carcinoma andbasal cell carcinoma.
复制标题
睑板腺癌和基底细胞癌的不同衰老能力。
DOI：
10.1002/ijc.29882
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发表时间：
2016
影响因子：
6.4
通讯作者：
黄筱琳
中科院分区：
文献类型：
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作者：
黄筱琳
睑板腺癌（MGC）和基底细胞癌（BCC）是常见的眼睑癌，表现出高度不同程度的增殖和转移。我们在这里解决的问题，这两个眼睑癌之间的差异机制，解释其不同的结果。共分析了102例确诊的MGC和175例确诊的BCC病例。收集了20例确诊的MGC和20例确诊的BCC病例，以确定端粒长度、衰老细胞的存在以及端粒加帽shelterin复合物、P53和E3泛素连接酶Siah 1的表达水平。在MGC和BCC中均检测到shelterin亚基蛋白水平降低、端粒长度缩短、Ki-67和Bcl 2过表达以及P53突变。提示shelterin复合物蛋白水平的降低和端粒长度的缩短与MGC和BCC的发生有关。然而，有几个参数区分MGC和BCC样品：（i）MGC中shelterin亚基的mRNA水平降低，但BCC中增加;（ii）MGC中P53突变更高;（iii）BCC中Siah 1 mRNA过表达;（iv）BCC样品含有更高水平的衰老细胞;（v）BCC中Ki-67和Bcl 2表达较低。这些结果支持了一个模型，其中与MGC相比，BCC中的P53检查点缺失导致细胞衰老和肿瘤增殖减少。
Meibomian gland carcinoma (MGC) and basal cell carcinoma (BCC) are common eyelid carcinomas that exhibit highly dissimilar degrees of proliferation and prognoses. We address here the question of the differential mechanisms between these two eyelid cancers that explain their different outcome. A total of 102 confirmed MGC and 175 diagnosed BCC cases were analyzed. Twenty confirmed MGC and twenty diagnosed BCC cases were collected to determine the telomere length, the presence of senescent cells, and the expression levels of the telomere capping shelterin complex,P53, and the E3 ubiquitin ligaseSiah1. Decreased protein levels of the shelterin subunits, shortened telomere length, over‐expressed Ki‐67, and Bcl2 as well as mutations inP53were detected both in MGC and BCC. It suggests that the decreased protein levels of the shelterin complex and the shortened telomere length contribute to the tumorigenesis of MGC and BCC. However, several parameters distinguish MGC from BCC samples: (i) the mRNA level of the shelterin subunits decreased in MGC but it increased in BCC; (ii)P53was more highly mutated in MGC; (iii)Siah1mRNA was over‐expressed in BCC; (iv) BCC samples contain a higher level of senescent cells; (v) Ki‐67 and Bcl2 expression were lower in BCC. These results support a model where a preservedP53checkpoint in BCC leads to cellular senescence and reduced tumor proliferation as compared to MGC.