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

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.

Effects of the box-3 region of the LIFRalpha-chain cytoplasmic domain (gp190CT3) on the proliferation and differentiation of HL-60 cells / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the effects of Box-3 region of the leukemia inhibitory factor receptor (LIFR) alpha-chain cytoplasmic domain on the proliferation and differentiation of HL-60 cells.</p><p><b>METHODS</b>Expression vector of gp190CT3 was constructed and expressed in HL-60 cells. The expression level of gp190CT3 was assayed by immunocytochemistry. The growth of wild type and gp190CT3 transfected HL-60 cells were examined under microscope. The PCNA levels were assayed by Western blot, and the levels of CD15 by flow cytometry.</p><p><b>RESULTS</b>The gp190CT3 transfected HL-60 cells were enlarged in size and their proliferation was slower than that of wild type. The expression level of PCNA was down-regulated while the level of CD15 up-regulated in transfected HL-60 cells as compared with that of the wild type cells.</p><p><b>CONCLUSION</b>The Box-3 region of the leukemia inhibitory factor receptor alpha-chain cytoplasmic domain (gp190CT3) participates the LIFR signal transduction in inhibiting the growth and inducing the differentiation of HL-60 cells.</p>