Mengying Huang, Ph.D.

Mengying Huang, Ph.D.
Postdoctoral fellow, Shi Laboratory


Dr. Mengying Huang earned her B.Sc. in biotechnology, her M.Sc. in cell biology and her Ph.D. in biochemistry and molecular biology from Southwest University. While there, much of her research focused on elucidating the mechanisms underlying brain cancers, specifically glioblastoma and neuroblastoma. In 2018, she joined the lab of Dr. Xiaobing Shi at UT MD Anderson Cancer and, in April of that year, moved to Van Andel Institute along with the Shi Laboratory. Her primary research focus is to identify and characterize novel readers of histone modifications.



Current research focus

H2A.Z is a histone H2A variant, which is conserved in all eukaryotes and is a genome-wide signature of nucleosomes at promoters and enhancers. H2A.Z is important for regulating gene expression, gene silencing boundaries, DNA repair, cell cycle progression and chromosome stability. DNA methylation is a process by which methyl groups are added to the DNA molecule, usually cytosine at the CpG site. Methylation can change the activity of a DNA segment without changing the sequence. When located in a gene promoter, DNA methylation typically acts to repress gene transcription. DNA methylation is essential for normal development and is associated with a number of key processes including genomic imprinting, X-chromosome inactivation, repression of transposable elements, aging and carcinogenesis. H2A.Z deposition is a H2A replacement. There is an interesting antagonism between H2A.Z deposition and DNA methylation. We are investigating the factors that regulate this and aim to elucidate the underlying mechanism.

Education & training

Postdoctoral fellow, Department of Epigenetics and Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center (Advisor: Dr. Xiaobing Shi)

Ph.D. in biochemistry and molecular biology, Southwest University (Advisor: Dr. Hongjuan Cui)
Thesis: Investigation of the role of MINA in glioblastoma cell proliferation and tumorigenesis and the underlying mechanisms

M.Sc. in cell biology, Southwest University (Advisor: Dr. Hongjuan Cui)

B.Sc. in biotechnology, Southwest University


National Scholarship of China (2016)

Social Work Award of Southwest University (2015)

Outstanding Graduate Cadres of Southwest University (2013)

Outstanding Graduate of Southwest University (2012)

Outstanding Intern of Southwest University (2012)

Third-Class Scholarship of Southwest University (2011)

Second-Class Scholarship of Southwest University (2010)

Self-Reliance Advanced Individual Award of Southwest University (2009)


Xuan F, Huang M, Zhao E, Cui H*. 2018. MINA53 deficiency leads to glioblastoma cell apoptosis via inducing DNA replication stress and diminishing DNA damage response. Cell Death Dis 9(11):1062.

Huang M, Xuan F, Liu W, Cui HJ*. 2017. MINA controls proliferation and tumorigenesis of glioblastoma by epigenetically regulating cyclins and CDKs via H3K9me3 demethylation. Oncogene 36(3):387–396.

Yang L*, Huang M*, Tan J, Hou J, He J, Wang F, Cui G, Yi L. 2017. Transcriptional co-activator with PDZ-binding motif overexpression promotes cell proliferation and transcriptional co-activator with PDZ-binding motif deficiency induces cell cycle arrest in neuroblastoma. Oncol Lett 13(6):4295–4301.

Xuan F, Huang M, Liu W, Ding H, Yang L, Cui H. 2016. Homeobox C9 suppresses Beclin1-mediated autophagy in glioblastoma by directly inhibiting the transcription of death-associated protein kinase 1. Neuro Oncol 18(6):819–829.

Yan X, Ke XX, Zhao H, Huang M, Hu R, Cui H. 2015. Triptolide inhibits cell proliferation and tumorigenicity of human neuroblastoma cells. Mol Med Rep 11(2):791–796.

Vinader V, Sadiq M, Sutherland M, Huang M, Loadman PM, Elsalem L, Shnyder SD, Cui H, Afarinkia K, Searcey M, Patterson LH, Pors K. 2015. Probing cytochrome P450-mediated activation with a truncated azinomycin analogue. Med Chem Commun 6:187–191.