Results
| PMID | 25625784 |
| Gene Name | MIR29C |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 30 |
| Population details | 30 (20 women with endometriosis, 10 samples of endometrium from women with hysteromyoma) |
| Age | 25 to 42 yrs |
| Sex | Female |
| Other associated phenotypes |
Endometriosis |
|
Int J Mol Med. 2015 Apr;35(4):1119-25. doi: 10.3892/ijmm.2015.2082. Epub 2015 Jan Long, Mei| Wan, Xiaohui| La, Xiaolin| Gong, Xiaoyun| Cai, Xia Productive Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uygur Autonomous Region 830054, P.R. China.| Department of Gynaecology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uy 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 knowledge, 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. Mesh Terms: Apoptosis/*genetics| Cell Line| Cell Movement/genetics| Cell Proliferation| Down-Regulation| Endometriosis/*genetics| Endometrium/*metabolism| Female| Gene Expression| *Gene Expression Regulation| Humans| MicroRNAs/chemistry/*genetics| Proto-O |
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