miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun
miR-29c is downregulated in the ectopic endometrium and exerts its effects on endometrial cell proliferation, apoptosis and invasion by targeting c-Jun
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DOI：
10.3892/ijmm.2015.2082
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发表时间：
2015-04-01
影响因子：
5.4
通讯作者：
Cai, Xia
中科院分区：
文献类型：
--
作者：
Long, Mei;Wan, Xiaohui;Cai, Xia
子宫内膜异位症是一种普遍而复杂的妇科疾病，影响10%的育龄妇女。一些研究表明，大量的microRNAs （miRNAs或miRs）在异位子宫内膜中异常或差异表达。到目前为止，据我们所知，还没有关于miR-29在子宫内膜中的作用的报道。在本研究中，我们通过逆转录-定量聚合酶链反应（RT-qPCR）研究了miR-29家族在无子宫内膜异位症女性子宫内膜样本以及配对异位和异位子宫内膜样本中的表达。结果显示miR-29c在配对的异位和异位子宫内膜样本中存在差异表达。此外，通过western blot检测，c-Jun在异位和异位子宫内膜组织中表达差异。此外，我们还在体外研究了miR-29c在子宫内膜细胞增殖、侵袭和凋亡中的作用。结果表明，miR-29c通过抑制子宫内膜细胞的增殖和侵袭，促进细胞凋亡来作用于子宫内膜细胞。此外，我们发现c-Jun是miR-29c的新靶点，c-Jun逆转了miR-29c对子宫内膜细胞增殖、侵袭和凋亡的影响。据我们所知，这项研究首次发现miR-29c是子宫内膜异位症的抑制因子。综上所述，我们的研究结果表明，miR-29c通过抑制c-Jun的表达来影响子宫内膜细胞的增殖、凋亡和侵袭。我们的数据可能为子宫内膜异位症的治疗提供一个新的潜在的治疗靶点。
Endometriosis is a prevalent and complex gynecological disease which affects 10% of women of reproductive age. Certain studies have suggested that a substantial number of microRNAs (miRNAs or miRs) are aberrantly or differentially expressed in the ectopic endometrium. To date, to the best of our knowlewdge, there is no report available on the role of miR-29 in the endometrium. In this study, we investigated the expression of the miR-29 family in the endometrium samples from women without endometriosis, as well as in paired ectopic and eutopic endometrium samples by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results revealed that miR-29c was differentially expressed in the paired eutopic and ectopic endometrium samples. In addition, c-Jun was differentially expressed in the ectopic and eutopic endometrial tissues as determined by western blot analysis. Furthermore, the role of miR-29c in endometrial cell proliferation, invasion and apoptosis was examined in vitro. The results revealed that miR-29c exerted its effects on endometrial cells by suppressing cell proliferation and invasion, as well as promoting cell apoptosis. Furthermore, it was found that c-Jun was a novel target of miR-29c, and c-Jun reversed the effects of miR-29c on the proliferation, invasion and apoptosis of endometrial cells. To the best of our knowledge, this study is the first to identify miR-29c as a suppressor of endometriosis. Taken together, our results suggest that miR-29c exerts its effects on endometrial cell proliferation, apoptosis and invasion by inhibiting the expression of c-Jun. Our data may provide a novel potential therapeutic target for the treatment of endometriosis.