Directory > Faculty
Chengfeng Yang, M.D., Ph.D.
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Assistant Professor
Department of Physiology
Center for Integrative Toxicology
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4171 Biomedical Physical Sciences
Tel: 517-355-6475 x 1139
Fax: 517-355-5125
E-mail: yangcf@msu.edu
Education
2001: Ph.D. National University of Singapore, SINGAPORE
1986: M.D. Tongji Medical University, Wuhan, CHINA
Research Interests: My research focuses on three areas: (1) Chemical
carcinogenesis studies: Arsenic is one of the most common environmental
carcinogens and causes cancer in many organs, such as lung, skin,
liver, prostate and bladder. While the carcinogenicity of arsenic
has been recognized many years ago, the molecular mechanism by
which arsenic induces cancers have not been well understood. This
is mainly due to the lack of proper animal models for studying
arsenic carcinogenicity. The findings from our recent studies
and those of others show that arsenic can transform human immortalized
cells, which provides an alternative approach for investigating
molecular mechanisms of arsenic carcinogenesis. Results of recent
cell culture studies suggest that arsenic shares many properties
with tumor promoters. Our studies will examine the epigenetic
mechanism of arsenic carcinogenicity, identifying key signaling
molecules and pathways that play critical roles in arsenic-induced
cell transformation and carcinogenesis; (2) Cancer biology studies:
Studies have shown that the active small Rho GTPases interact
with various effectors to initiate downstream signaling events
that control the processes of actin cytoskeleton reorganization,
adhesion, migration, gene expression, cell survival, proliferation,
and malignant transformation. Although Rho GTPases have been implicated
in various cancers, particularly in breast cancer, a strong causative
link between Rho GTPases and primary human cancers has not yet
been established. Our recent studies show that Rac1, a member
of the Rho GTPase family, plays a key role in growth factor (heregulin
beta1)-triggered breast cancer cell migration and proliferation.
Future studies will investigate the molecular mechanisms by which
Rac1 and other small GTPases regulate gene expression, cell survival
and proliferation, and determine their role in growth factor/hormone
oncogenic signaling, and in cancer development/progression; (3)
Cancer prevention and therapy sensitization studies: drug resistance
and toxicities are major reasons responsible for the failure of
effective cancer treatment. We are interested in identifying naturally
occurring compounds that are capable of selectively killing cancer
cells or reversing drug resistance, and preventing environment
carcinogen-induced carcinogenesis.
Selective Publications
1. Yang, C., Klein, E.A., Assoian, R.K. and Kazanietz, M.G. Heregulin
promotes breast cancer cell proliferation via Rac/Erk-dependent
induction of cyclin D1 and p21cip1. Biochem. J. (in press) 2007.
2. Yang, C., and Kazanietz, M.G. Chimaerins: GAPs that bridge
diacylglycerol signaling and the small G-protein Rac. Biochem.
J. 403: 1-12. 2007.
3. Klein, E. A., Yang, C., Kazanietz, M.G. and Assoian, R.K.
NFkB-Independent Signaling to the Cyclin D1 Gene by Rac. Cell
Cycle 6: 1115-1121. 2007.
4. Wang, H., Yang, C., Coluccio Leskow, F., Sun, J., Canagarajah,
B., Hurley, J.H., and Kazanietz, M.G. Phospholipase C/diacylglycerol-dependent
activation of B2-chimaerin restricts EGF-induced Rac signaling.
EMBO J. 25, 2062-2074, 2006.
5. Yang, C., Liu Y., Lemmon, M.A., and Kazanietz, M.G. Essential
role for Rac in heregulin B1 mitogenic signaling in breast cancer
cells: a novel mechanism that involves EGFR and is independent
of ErbB4. Mol. Cell. Biol. 26, 831-842, 2006.
6. Yang, C., Liu Y, Coluccio Leskow F, Weaver VM, Kazanietz MG.
Rac-GAP-dependent inhibition of breast cancer cell proliferation
by B2-chimaerin. J. Biol. Chem. 280, 24363-24370, 2005.
7. Yang, C., and Kazanietz, M.G. Divergence and complexities
in DAG signaling: looking beyond PKC. Trends Pharmacol. Sci. 24,
602-608, 2003.
8. Yang, C., Wu, J., Zhang, R., Zhang, P., Eckard, J., Yusuf,
R., Huang, X., Rossman, T.G., and Frenkel K. Caffeic acid phenethyl
ester (CAPE) prevents transformation of human cells by arsenite
(As) and suppresses growth of As-transformed cells. Toxicology
213, 81-96, 2005.
9. Dai, J., Huang, C., Wu, J., Yang, C., Frenkel, K., and Huang,
X. Iron-induced interleukin-6 gene expression: possible mediation
through the extracellular signal-regulated kinase and p38 mitogen-activated
protein kinase pathways. Toxicology 203, 199-209, 2004.
10. Yang, C., and Frenkel, K. Arsenic-mediated cellular signal
transduction, transcription factor activation and aberrant gene
expression–implications in carcinogenesis. J. Environ. Path. Toxicol.
Oncol. 21: 331-342, 2002.
11. Zhang, S., Lin, Z.N., Yang, C., Shi, X., Ong, C.N., and Shen,
H.M. Suppressed NF-kB and sustained JNK activation contribute
to the sensitization effect of parthenolide to TNF–α induced apoptosis
in human cancer cells. Carcinogenesis 25, 2191-2199, 2004
12. Liu, J., Yang, C., Wasser, S., Shen, H.M., Tan, C.E.L., and
Ong, C.N. Protection of Salvia Miltiorrhiza against aflatoxin
B1-induced hepatocarcinogenesis in Fisher 344 rats: Dual mechanisms
involved. Life Sciences 69, 309-326, 2001.
13. Shen, H.M., Yang, C., Ding W.X., Liu, J., and Ong, C.N. Superoxide
radical-initiated apoptotic signaling pathway in selenite-treated
HepG2 cells: Mitochondria serve as the main target. Free Radical
Biol. Med. 30, 9-21, 2001.
14. Yang, C., Liu, J., Wasser, S., Shen, H.M., Tan, C.E.L., and
Ong, C.N. Inhibition of ebselen on aflatoxin B1-induced hepatocarcinogenesis
in Fisher 344 rats. Carcinogenesis 21, 2237-2243, 2000.
15. Yang, C., Shen, H.M., and Ong, C.N. Intracellular thiol depletion
causes mitochondrial permeability transition in ebselen-induced
apoptosis. Arch. Biochem. Biophys. 380, 319-330, 2000.
16. Yang, C., Shen, H.M., and Ong, C.N. Ebselen-induces apoptosis
in HepG2 cells through rapid depletion of intracellular thiols.
Arch. Biochem. Biophys.374, 142-152, 2000.
17. Yang C., Liu J., Shen H.M., and Ong C.N. Protective effect
of ebselen on aflatoxin B1-induced oxidative damage in primary
rat hepatocytes. Pharmacol. Toxicol. 86, 156-161, 2000.
18. Shen, H.M., Yang, C., Liu, J., and Ong, C.N. Dual-role of
glutathione in selenite induced oxidative stress and apoptosis
in human hepatoma cells (HepG2). Free Radical Biol. Med. 28, 1115-1124,
2000.
19. Yang, C., Shen, H.M., and Ong, C.N. Protective effect of
ebselen against hydrogen peroxide-induced cytotoxicity and DNA
damage in HepG2 cells. Biochem. Pharmacol. 57, 273-279, 1999.
20. Shen, H.M., Yang, C., and Ong, C.N. Sodium selenite-induced
oxidative damage and apoptosis in human hepatoma HepG2 cells.
Int. J. Cancer 81, 820-828, 1999.
21. Liu, J., Yang, C., Shen, H.M., and Ong, C.N. Protective effect
of Salvia Miltiorrhiza on aflatoxin B1-induced cytotoxicity in
rat primary hepatocytes. Free Radical Res. 31, 559-568, 1999.
22. Yang, C., Shen, H.M., Shen, Y., Zhuang, Z.X., and Ong C.N.
Cadmium-induced oxidative cellular damage in human fetal lung
fibroblasts (MRC-5 cells). Envrion. Health Perspect. 105, 712-716,
1997.
Other Publications
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