Fei Chen

Fei Chen


(313) 577-9201


Fei Chen


EACPHS, Wayne State University 259 Mack Avenue, Detroit, MI 48201

Office Address

EACPHS, Wayne State University
259 Mack Avenue, Detroit, MI 48201


Department of Pharmaceutical Sciences

Research Interests

• Cancer cell biology and pharmaceutics
• Environmental risk factors and epigenetics
• Intracellular metabolism and Cancer stem cells
• Histone methylation and lung cancer

Research Description

The broad focus of the Chen lab is to investigate genetic and epigenetic regulations of genes in human cancers 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 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 environmental arsenic exposure shifts the intracellular metabolic program from mitochondrial TCA cycle to glycolysis, and how this shift in metabolism contributes to the change or reset of the epigenetic landscape on chromatin, and the generation of the cancer stem cells.

Selected Publications

Bi Z, Zhang Q, Fu Y, Wadgaonkar P, Zhang W, Almutairy B, Xu L, Rice M, Qiu Y, Thakur C, Chen F*. Nrf2 and HIF1α converge to arsenic-induced metabolic reprogramming and the formation of the cancer stem-like cells. Theranostics. 2020;10:4134-49.

Zhang Q, Thakur C, Fu Y, Bi Z, Wadgaonkar P, Liu Z, Liu W, Wang J, Kidder BL, Chen F*. Mdig promotes oncogenic gene expression through antagonizing repressive histone methylation markers. Theranostics. 2020;10:602-14.

Chen F*. Linking metabolism to epigenetics in stem cells and cancer stem cells (Editorial). Seminars in Cancer Biology. 2019;57:iii-v.

Thakur C, Chen F*. Connections between metabolism and epigenetics in cancers. Seminars in Cancer Biology. 2019;57:52-8.

Zhang Q, Thakur C, Shi J, Sun J, Fu Y, Stemmer P, Chen F*. New discoveries of mdig in the epigenetic regulation of cancers. Seminars in Cancer Biology. 2019;57:27-35.

Thakur C, Chen B, Li L, Zhang Q, Yang ZG, Chen F*. Loss of mdig expression enhances DNA and histone methylation and metastasis of aggressive breast cancers. Signal Traduction and Targeted Therapy. 2018;3:25.

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.


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

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