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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>
AGR2, a mucinous ovarian cancer marker, promotes cell proliferation and migration
이제호,Kyoungsook Park,Yong Jin Chung,Hyekyung So,김광수,박준수,Mijoung Oh,Minwha Jo,Kyusam Choi,이은주,Yoon-La Choi,Sang Yong Song,배덕수,김병기 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.2
Ovarian cancer is a leading cause of death in women. Early detection of ovarian cancer is essential to decrease mortality. However, the early diagnosis of ovarian cancer is difficult due to a lack of clinical symptoms and suitable molecular diagnostic markers. Thus,identification of meaningful tumor biomarkers with potential clinical application is clearly needed. To search for a biomarker for the early detection of ovarian cancer,we identified human anterior gradient 2 (AGR2)from our systematic analysis of paired normal and ovarian tumor tissue cDNA microarray. We noted a marked overexpression of AGR2 mRNA and protein in early stage mucinous ovarian tumors compared to normal ovarian tissues and serous type ovarian tumors by Western blot analysis and immunohistochemistry. To further elucidate the role of AGR2 in ovarian tumorigenesis,stable 2774 human ovarian cancer cell lines overexpressing AGR2 were established. Forced expression of AGR2 in 2774 cells enhanced the growth and migration of ovarian cancer cells. AGR2 protein was detected in the serum of mucinous ovarian cancer patients by Western blot and ELISA analysis. Thus,AGR2 is a potential biomarker for the diagnosis of mucinous ovarian cancer and an ELISA assay may facilitate the early detection of mucinous ovarian cancer using patient serum.