Fei Chen


Fei Chen, Ph.D.
Department of Pharmaceutical Sciences
EACPHS, Wayne State University
259 Mack Avenue, Detroit, MI 48201
(313) 577-9201

Research Interests:
• Cancer cell biology and pharmaceutics
• Cancer signaling and epigenetics
• Cancer stem cells and miRNAs
• Histone methylation and lung cancer
• JNK, Stat3, Akt, EZH2, and stem cell reprogramming

Research Description:
The broad focus of the Chen lab is to investigate genetic and epigenetic regulations of genes in human lung cancer related to environmental or occupational exposure to mineral dust and carcinogenic metals. More specifically, the lab employs biochemical approaches to elucidate molecular mechanisms by which the expression and function of genes contributing to lung inflammation and tumorigenesis are altered. One of the key signaling events in carcinogenic gene regulation is the activation of kinases and transcription factors, such as JNK, Stat3, Akt, and NF-kappaB. A principal question to be addressed is how extracellular inducers, such as reactive oxygen species (ROS), cytokines and carcinogenic metals, perturb the intracellular regulatory circuits that control cross-talk, durability and potency of the kinase pathways.

Accumulating evidence suggests that many environmental factors contribute to malignant transformation of the cells through altering intracellular signaling pathways that converge on epigenetic regulation, such as methylation of the histone proteins and DNA, acetylation and ubiquitination of the histone proteins. The status of histone methylation, especially on the N-terminal tails of histones H3 and H4, directly determines the accessibility of the regulatory factors on the genes packed in the condensed chromatin fibers. The Chen lab had previously identified a mineral dust-induced gene, mdig that contains a signature motif of histone demethylases, the JmjC domain. The current effort is to determine whether this gene product possesses the demethylase activity or affects methylation status of the histone proteins through interaction with other nuclear proteins. An addition project is to study how arsenic-activated JNK, Stat3 and Akt regulate expression of miRNAs and phosphorylation of EZH2 that linked to self-renewal of the cancer stem cells.

Selected Publications:

Li L, Chen F. Arsenic and SUMO wrestling in protein modification. Cell Cycle. 2017;16:913-4.

Zhang D, Wang F, Pang Y, Zhao E, Zhu S, Chen F, Cui H. ALG2 regulates glioblastoma cell proliferation, migration and tumorigenicity.  Biochem Biophys Res Commun. 2017;486:300-6.

Wu K, Li L, Thakur C, Lu Y, Zhang X, Yi Z, Chen F. Proteomic Characterization of the World Trade Center dust-activated mdig and c-myc signaling circuit linked to multiple myeloma. Sci Rep. 2016;6:36305.

McDermott JR, Geng X, Jiang L, Gálvez-Peralta M, Chen F, Nebert DW, Liu Z. Zinc- and bicarbonate-dependent ZIP8 transporter mediates selenite uptake. Oncotarget. 2016;7:35327-40.

Li L, Chen F. Oxidative stress, epigenetics, and cancer stem cells in arsenic carcinogenesis and prevention. Curr Pharmacol Rep. 2016;2:57-63.

Education and Training


1979-1982 Medicine, Nantong Medical College, China
1989-1994 PhD in Immunology, Peking University Health Sciences Center, China
1994-1998 Postdoctoral Fellow, Penn State University, Hershey, Pennsylvania