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Mei-Yi Wu Mei-Yi Wu
Adjunct Associate Professor of Anatomy and Cell Biology

Office Phone: 202-994-3511
Email: Email
Department: Anatomy and Cell Biology


My research focus is using mouse models to study how gene mutation contributes to the development of human diseases, including leukemia (and other cancers), infertility, and kidney diseases. Recently, we have identified two related genes, Arid4a and Arid4b, as new members of chromatin remodeling genes. To study their roles in human diseases, we generated knockout mice carrying mutations (deletions) of Arid4a and Arid4b. Using these Arid4a and Arid4b mouse as a model system, we found that mutations in these genes contribute to development of human diseases and cancer through epigenetic mechanisms. Deficiency of Arid4a and Arid4b in mice leads to a hematopoietic disorder with striking similarity to the course of events found in human leukemia. Our results suggest that Arid4a and Arid4b act as tumor suppressor genes with a prominent role in leukemic transformation. Using this mouse model, we recently found that Arid4a and Arid4b function in urogenital development. We now also study whether Arid4a and Arid4b play a role in the regulation of gonadal tumorigenesis, as well as breast cancer and prostate cancer. To further investigate how genetic abnormalities can generate secondary epigenetic effects in disease states, we study the regulatory molecular mechanisms of Arid4a and Arid4b by identifying targeting genes and characterize their regulatory impact of epigenetic effects on the downstream genes. Our discoveries will increase the potential to understand and treat disease conditions. These studies will also contribute significantly to our understanding of the connection between gene regulation, epigenetic control, disease development, and cancer formation.


Mei-Yi Wu, Junjiang Fu, Xiuli Xiao, Jingbo Wu, and Ray-Chang Wu. MiR-34a Regulates Therapy Resistance by Targeting HDAC1 and HDAC7 in Breast Cancer. Cancer Letters, 2014 (in press).

Wu R.C., Jiang M., Beaudet A.L., and Wu M.Y.* (2013) ARID4A and ARID4B regulate male fertility, a functional link to the AR and RB pathways. Proc Natl Acad Sci U S A. (in press) *corresponding author

Wu, M.Y., Fu, J., Xu, J., O’Malley, B.W., and Wu R.C. Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor. Cell Research. 2012, in press.

Wu, M.Y., Jiang, M., Zhai, X., Beaudet, A., and Wu, R.C. An Unexpected Function of the Prader-Willi Syndrome Imprinting Center in Maternal Imprinting in Mice. PLoS One, in press. 2012.

Wu M.Y., Eldin K., and Beaudet, A.L. (2008) Chromatin remodeling genes Arid4a and Arid4b function as leukemia suppressor genes. J Natl Cancer Inst 100(17):1247-59. PMID: 18728284

Wu M.Y., Tsai, T.F., and Beaudet, A.L. (2006) Deficiency of Rbbp1/Arid4a and Rbbp1l1/Arid4b alters epigenetic modifications and suppresses animprinting defect in the PWS/AS domain. Genes Dev. 20(20):2859-70. PMID: 17043311

Wu M.Y., Chen K.S., Bressler, J., Hou A., Tsai, T.F., and Beaudet, A.L. (2006) Mouse imprinting defect mutations that model Angelm syndrome. Genesis 44(1):12-22. PMID: 16397868

Bressler, J., Tsai, T.F., Wu M.Y., Tsai, S.F., Ramirez, M.A., Armstrong, D., and Beaudet, A.L. (2001) The SNRPN promoter is not required for genomicimprinting of the Prader-Willi/Angelman domain in mice. Nature Genetics 28(3):232-40. PMID: 11431693

Wu, M.Y., Wang, P.Y., Han, S.H. and Hsieh, S.L. (1999) The cytoplasmic domain of lymphotoxin-? receptor mediates cell death in HeLa cells. J. Biol. Chem. 274(17):11868-11873. PMID: 10207006

Wu, M.Y., Hsu, T.L., Lin, W.W., Capmbell, R.D., and Hsieh, S.L. (1997) Serine/threonine kinase activity associated with the cytoplasmic domain of lymphotoxin-? receptor in HepG2 cells. J. Biol. Chem. 272(27):17154-9. PMID: 9202035

Industry Relationships and Collaborations

This faculty member (or a member of their immediate family) has reported a financial interest with the health care related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.

  • None