Mitochondrial DNA content and mass increase in progression from normal to hyperplastic to cancer endometrium.

Mitochondrial DNA content and mass increase in progression from normal to hyperplastic to cancer endometrium.
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DOI:
10.1186/1756-0500-5-279
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发表时间:
2012-06-07
期刊:
影响因子:
1.8
通讯作者:
Gadaleta MN
Gadaleta MN
中科院分区:
其他
文献类型:
--
作者:
Cormio A;Guerra F;Cormio G;Pesce V;Fracasso F;Loizzi V;Resta L;Putignano G;Cantatore P;Selvaggi LE;Gadaleta MN

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线粒体DNA (mtDNA)含量和线粒体生物发生的增加与PGC-1α信号通路的激活有关,此前曾报道过I型子宫内膜癌。本研究的目的是评估mtDNA含量和柠檬酸合酶(CS)活性(一种线粒体质量的酶标记物)在从对照子宫内膜到增生到I型子宫内膜癌的进展过程中是否增加。鉴于在月经周期的不同阶段或绝经期子宫内膜中发现mtDNA含量和CS活性没有统计学意义的变化,因此将这些样本作为对照。我们的研究首次表明,与对照组织相比,增生性子宫内膜的mtDNA含量和柠檬酸合成酶活性有所增加,尽管它们的水平仍低于癌组织。特别是,mtDNA含量的增加似乎先于CS活性的增加。mtDNA含量和CS活性与不同的组织病理条件(如分级、子宫内膜浸润和分期)没有统计学意义的变化。MtDNA含量和柠檬酸合成酶活性在癌前病变中升高可能是增生到癌进展的潜在分子标记。
An increase in mitochondrial DNA (mtDNA) content and mitochondrial biogenesis associated with the activation of PGC-1α signalling pathway was previously reported in type I endometrial cancer. The aim of this study has been to evaluate if mtDNA content and the citrate synthase (CS) activity, an enzyme marker of mitochondrial mass, increase in progression from control endometrium to hyperplasia to type I endometrial carcinoma. Given that no statistically significant change in mtDNA content and CS activity in endometrium taken from different phases of the menstrual cycle or in menopause was found, these samples were used as control. Our research shows, for the first time, that mtDNA content and citrate synthase activity increase in hyperplastic endometrium compared to control tissues, even if their levels remain lower compared to cancer tissue. In particular, mtDNA content increases seem to precede increases in CS activity. No statistically significant change in mtDNA content and in CS activity was found in relation to different histopathological conditions such as grade, myometrial invasion and stage. MtDNA content and citrate synthase activity increases in pre-malignant lesions could be a potential molecular marker for progression from hyperplasia to carcinoma.