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Chae, Myounghee,Rhee, Gyu-Seek,Jang, Ik-Soon,Kim, Kwangsoo,Lee, Ji-Hae,Lee, Seung-Yeul,Kim, Minjung,Yang, Junyoung,Park, Junsoo,Lee, Seung-Hoon Springer-Verlag 2009 Molecules and cells Vol.27 No.5
<P>The amphetamine derivative 3, 4-methylenedioxymethamphetamine (MDMA) has become a popular recreational drug, and has also been shown to cause serotonergic neurotoxicity. This report shows that MDMA impairs brain development in a whole mouse embryo culture. The results of quantitative real-time PCR analysis showed that autophagy-related protein 5 (Atg5) expression is elevated in mouse embryo and neuroblastoma cells after MDMA treatment. This elevated Atg5 expression interferes with the neuronal differentiation of neuroblastoma cells such as SH-SY5Y and PC12 cells. Thus, our results suggest that the use of MDMA during pregnancy may impair neuronal development via an induction of Atg5 expression.</P>
Myounghee Chae,Gyu-Seek Rhee,장익순,김광수,Ji-Hae Lee,Seung-Yeul Lee,Minjung Kim,Junyoung Yang,박준수,이승훈 한국분자세포생물학회 2009 Molecules and cells Vol.27 No.5
The amphetamine derivative 3, 4-methylenedioxymetham- phetamine (MDMA) has become a popular recreational drug, and has also been shown to cause serotonergic neurotoxicity. This report shows that MDMA impairs brain development in a whole mouse embryo culture. The results of quantitative real-time PCR analysis showed that autophagy-related protein 5 (Atg5) expression is elevated in mouse embryo and neuroblastoma cells after MDMA treatment. This elevated Atg5 expression inter-feres with the neuronal differentiation of neuroblastoma cells such as SH-SY5Y and PC12 cells. Thus, our results suggest that the use of MDMA during pregnancy may impair neuronal development via an induction of Atg5 expression.
Dkk3, downregulated in cervical cancer, functions as a negative regulator of β-catenin
Lee, Eun-Ju,Jo, Minwha,Rho, Seung Bae,Park, Kyoungsook,Yoo, Yae-Na,Park, Junsoo,Chae, Myounghee,Zhang, Wei,Lee, Je-Ho Wiley Subscription Services, Inc., A Wiley Company 2009 International journal of cancer: Journal internati Vol.124 No.2
<P>The Wnt/β-catenin signaling pathway is activated during the malignant transformation of keratinocytes that originate from the human uterine cervix. Dkk1, 2 and 4 have been shown to modulate the Wnt-induced stabilization of the β-catenin signaling pathway. However, the function of Dkk3 in this pathway is unknown. Comparison of the Dkk3 gene expression profiles in cervical cancer and normal cervical tissue by cDNA microarray and subsequent real-time PCR revealed that the Dkk3 gene is frequently downregulated in the cancer. Methylation studies showed that the promoter of Dkk3 was methylated in cervical cancer cell lines and 22 (31.4%) of 70 cervical cancer tissue specimens. This promoter methylation was associated with reduced expression of Dkk3 mRNA in the paired normal and tumor tissue samples. Further, the reintroduction of Dkk3 into HeLa cervical cancer cells resulted in reduced colony formation and retarded cell growth. The forced expression of Dkk3 markedly attenuated β-catenin-responsive luciferase activity in a dose-dependent manner and decreased the β-catenin levels. By utilizing a yeast two-hybrid screen, βTrCP, a negative regulator of β-catenin was identified as a novel Dkk3-interacting partner. Coexpression with βTrCP synergistically enhanced the inhibitory function of Dkk3 on β-catenin. The stable expression of Dkk3 blocks the nuclear translocation of β-catenin, resulting in downregulation of its downstream targets (VEGF and cylcin D), whereas knockdown of Dkk3 abrogates this blocking. We conclude from our finding that Dkk3 is a negative regulator of β-catenin and its downregulation contribute to an activation of the β-catenin signaling pathway. © 2008 Wiley-Liss, Inc.</P>