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DOI 10.3802/jgo.2008.19.2.139

Медицинская библиотека · Journal of gynecologic oncology · 2008

Tenascin-X and leukemia inhibitory factor receptor are down-regulated in leiomyoma compared with normal myometrium.

Lee Sun Ok, Lee Soo Yoon, Lee Sa Ra, Ju Woong, Kim Seung Cheol

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Аннотация

OBJECTIVE

Uterine leiomyomas are the most common tumor of the uterus. But the molecular causes of uterine leiomyoma remain unclear. We conducted the current investigation in order to elucidate the molecular mechanisms in the development of uterine leiomyoma.

METHODS

We employed a new and accurate reverse transcription-polymerase chain reaction (RT-PCR) method that involved annealing control primers (ACPs) to identify the genes that are differently expressed in uterine leiomyoma.

RESULTS

Using 120 ACPs, we identified and sequenced 14 differently expressed genes (DEGs) in uterine leiomyoma compared with normal myometrium. Basic Local Alignment Search Tool (BLAST) searches were performed to examine the known functions of these genes associated with uterine leiomyoma. We confirmed differently expressed patterns in more cases using the RT-PCR method. We also detected two novel genes, Tenascin-X and Leukemia Inhibitory Factor Receptor (LIFR), which had not yet been reported to have any functions associated with uterine leiomyoma. RT-PCR confirmation shows that both of these two genes are down-regulated in uterine leiomyoma.

CONCLUSION

Our results suggest that Tenascin-X and LIFR may play a role in the development of uterine leiomyoma. Although further studies are required to establish the precise mechanisms with which these genes are involved in the genesis of uterine leiomyoma, the present research is significant in that it is the first study which detects down-regulated novel genes in uterine leiomyoma using the ACP system.

Для цитирования: Lee Sun Ok, Lee Soo Yoon, Lee Sa Ra, Ju Woong, Kim Seung Cheol. Tenascin-X and leukemia inhibitory factor receptor are down-regulated in leiomyoma compared with normal myometrium.. Journal of gynecologic oncology. 2008. DOI: 10.3802/jgo.2008.19.2.139.
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