Access the full text.
Sign up today, get DeepDyve free for 14 days.
Xiaoyue Chen, Qin Yan, Shuangdi Li, Long Zhou, Hua-jing Yang, Yi-xia Yang, Xuelian Liu, X. Wan (2012)
Expression of the tumor suppressor miR-206 is associated with cellular proliferative inhibition and impairs invasion in ERα-positive endometrioid adenocarcinoma.Cancer letters, 314 1
B. Dey, J. Gagan, Anindya Dutta (2011)
miR-206 and -486 Induce Myoblast Differentiation by Downregulating Pax7Molecular and Cellular Biology, 31
L. Bally-Cuif, M. Gulisano, V. Broccoli, E. Boncinelli (1995)
c-otx2 is expressed in two different phases of gastrulation and is sensitive to retinoic acid treatment in chick embryoMechanisms of Development, 49
P. Mercier, Antonio Simeone, Franco Cotelli, Edoardo Boncinelli (1995)
Expression pattern of two otx genes suggests a role in specifying anterior body structures in zebrafish.The International journal of developmental biology, 39 4
(1994)
Positive and negative signals from mesoderm regulate the expression of mouse Otx 2 in ectoderm explants
D. Bartel (2009)
MicroRNAs: Target Recognition and Regulatory FunctionsCell, 136
C. Di, S. Liao, D. Adamson, T. Parrett, D. Broderick, Qun Shi, C. Lengauer, Jordan Cummins, V. Velculescu, D. Fults, R. McLendon, D. Bigner, Hai Yan (2005)
Identification of OTX2 as a medulloblastoma oncogene whose product can be targeted by all-trans retinoic acid.Cancer research, 65 3
M. Rhinn, A. Dierich, M. Meur, S. Ang (1999)
Cell autonomous and non-cell autonomous functions of Otx2 in patterning the rostral brain.Development, 126 19
Lin Gan, Chai Mao, A. Wikramanayake, L. Angerer, R. Angerer, William Klein (1995)
An orthodenticle-related protein from Strongylocentrotus purpuratus.Developmental biology, 167 2
S. Ang, Ronald Conlon, Ou Jin, Janet Rossant (1994)
Positive and negative signals from mesoderm regulate the expression of mouse Otx2 in ectoderm explants.Development, 120 10
RESEARCH ARTICLE Open Access Expression of miR-1, miR-133a, miR-133b and
Yong Zhao, D. Srivastava (2007)
A developmental view of microRNA function.Trends in biochemical sciences, 32 4
Yi Cui, Zhongji Han, Yi Hu, Ge Song, C. Hao, Hongfei Xia, Xu Ma (2012)
MicroRNA‐181b and microRNA‐9 mediate arsenic‐induced angiogenesis via NRP1Journal of Cellular Physiology, 227
R. Ibad, J. Rheey, S. Mrejen, V. Forster, S. Picaud, A. Prochiantz, K. Moya (2011)
Otx2 Promotes the Survival of Damaged Adult Retinal Ganglion Cells and Protects against Excitotoxic Loss of Visual Acuity In VivoThe Journal of Neuroscience, 31
(2005)
Identification of OTX 2 as a medulloblastoma oncogene whose product can be targeted by all - trans retinoic acid
J. Martínez-Barbera, M. Signore, P. Boyl, E. Puelles, D. Acampora, R. Gogoi, F. Schubert, A. Lumsden, A. Simeone (2001)
Regionalisation of anterior neuroectoderm and its competence in responding to forebrain and midbrain inducing activities depend on mutual antagonism between OTX2 and GBX2.Development, 128 23
Yi Cui, Zhongji Han, Yi Hu, Ge Song, C. Hao, Hongfei Xia, Maiyu Xu (2011)
Q 1 MicroRNA-181 b and microRNA-9 Mediate Arsenic-Induced Angiogenesis via NRP 1
J. Li, A. Joyner (2001)
Otx2 and Gbx2 are required for refinement and not induction of mid-hindbrain gene expression.Development, 128 24
M. Pannese, C. Polo, M. Andreazzoli, R. Vignali, Boris Kablar, G. Barsacchi, E. Boncinelli (1995)
The Xenopus homologue of Otx2 is a maternal homeobox gene that demarcates and specifies anterior body regions.Development, 121 3
T. Rosenquist, S. Ratashak, J. Selhub (1996)
Homocysteine induces congenital defects of the heart and neural tube: effect of folic acid.Proceedings of the National Academy of Sciences of the United States of America, 93 26
M. Rhinn, A. Dierich, W. Shawlot, Richard Behringer, M. Meur, S. Ang (1998)
Sequential roles for Otx2 in visceral endoderm and neuroectoderm for forebrain and midbrain induction and specification.Development, 125 5
A. Simeone, D. Acampora, A. Mallamaci, A. Stornaiuolo, M. D’Apice, Vincenzo Nigro, E. Boncinelli (1993)
A vertebrate gene related to orthodenticle contains a homeodomain of the bicoid class and demarcates anterior neuroectoderm in the gastrulating mouse embryo.The EMBO Journal, 12
V. Hamburger, H. Hamilton (1951)
A series of normal stages in the development of the chick embryoDevelopmental Dynamics, 195
MiR-206 was involved in a series of cellular activities, such as the growth and development of skeletal muscle and the tumorigenesis. MiR-206 was characterized previously as a differentially expressed gene in sodium arsenite (SA)-induced neural tube defects (NTDs) in chick embryos via miRNA microarray analysis. However, the role of miR-206 in the pathological process of nerve cells remained elusive. In this study we found differential expression of miR-206 in SA-treated chick embryos by Northern blot analysis. Ectopic expression of miR-206inhibited cell proliferation, and promoted cell apoptosis in U343 and SK-N-SH cell by using MTT, Edu Apollo assay and Flow cytometry analysis. Further investigation revealed that miR-206 can interact with 3′-untranslated region (UTR) of Otx2. MiR-206 mimics down-regulated the endogeneous Otx2 expression, whereas the miR-206 inhibitor obviously up-regulated the expression of Otx2. These findings indicate that overexpression of miR-206 promotes cell apoptosis and low expression of miR-206 inhibits cell apoptosis. Otx2 may play an important role in the process of miR-206-mediated cell apoptosis.
Cellular Physiology and Biochemistry – Karger
Published: Jan 1, 2012
Keywords: miR -206; Human Glioma Cells; Apoptosis; Otx2
Read and print from thousands of top scholarly journals.
Already have an account? Log in
Bookmark this article. You can see your Bookmarks on your DeepDyve Library.
To save an article, log in first, or sign up for a DeepDyve account if you don’t already have one.
Copy and paste the desired citation format or use the link below to download a file formatted for EndNote
Access the full text.
Sign up today, get DeepDyve free for 14 days.
All DeepDyve websites use cookies to improve your online experience. They were placed on your computer when you launched this website. You can change your cookie settings through your browser.