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I-Tsuen Chen

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I-Tsuen Chen, Ph.D.

Associate Professor 

 

Kansas State Univ.

Post Doctor training: Columbia Univ. & NIH 

TEL(office): +886-2-28267213

TEL(Lab): +886-2-28267000 ext5826

E-mail: chenit@ym.edu.tw

Dept. Biotechnology and Laboratory Science in Medicine 

National Yang Ming University, No. 155, Sec. 2, Linong St., Beitou District, Taipei City 112, Taiwan (R.O.C.)

 

 

Research Interests
We are interested in the role of tumor suppressor p53 and Rb in the regulation of cell cycle progression, apoptosis and DNA repair in response to DNA damage induced by anticancer agents, radiation and other genotoxic stress.

Current Projects
Protein modification such as phosphorylation play key role in signal pathways. A novel protein modification, Bcl-xL deamidation, induced by cisplatin has been observed in Rb-deficient cancer cells. Bcl-xL is a key regulator in intrinsic apopototic pathway. Deamidation of Bcl-xL alters its antiapoptotic properties and sensitizes tumor cells to cisplatin. By inactivating Rb with E1A, we are studying the signal pathways that lead to this modification in ovarian cancer cells. We have also demonstrated that ROS and NHE1 (Na+/H+ exchanger) are involved in Bcl-xL deamidation in liver cancer cells. Currently, we are searching additional genes involved in this pathway by DNA array analysis.

In addition, we are studying the effect of PIN1, a gene stabilizes cyclin D1, p53 etc., on cell’s senescence, apoptosis and radiation resistance by knockdown PIN1 expression. Interestingly, PIN1 knockdown reduces the expression of CD133, Sox-2 and c-Myc etc.., markers for cancer stem-like cells. Protein synthesis and cell growth are controlled by mTOR activity which is also suppressed by p53 and TSC2. We are also studying low energy and stresses on cell growth mediated by TSC2 and p53.

Selected Publications
1. E I-T Chen , J-R Wu, W-H Su, T-H Wang and L-C Au. Selective inhibition of p53 dominant negative mutation by shRNA resulting in partial restoration of p53 activity. (2009) J Med Sci, 29(4), 179-185.
2. Chang,CY, Lin, YM, Lee,WP, Hsu, HH and Chen, E.I.T.* (2006). Involvement of Bcl-XL deamidation in E1A-mediated cisplatin sensitization of ovarian cancer cells. Oncogene. 25, 2656-65.
3. Seo, Y.R., Chen, E.I.T. and Smith, M.L. (2002). Sensitivity of p53-deficient cells to oxaliplatin and thio-TEPA. Breast Cancer Res. Treat. 72:255-263.
4. Zhan, Q., Chen, I-T., Antinore, M. J. and Fornace, A.J. (1998). Tumor suppressor p53 can participate in transcriptional induction of the Gadd45 promoter in the absence of direct DNA binding. Mol. Cell. Biol. 18:2768-78.
5. Chen, I-T., Akamatsu, M., Smith, M.L., Lung, F.D., Duba. D., Roller, P.P., Fornace, Jr., A.J., and O'Connor, P. (1996). Characterization of p21Cip1/waf1 peptide domains required for cyclinE/Cdk2 and PCNA interaction. Oncogene. 12:595-607.
6. Chen, I-T., Smith, M.L., O'Connor, P. and Fornace, Jr. A.J. (1995). Direct interaction of Gadd45 with PCNA and evidence for competitive interaction of gadd45 and p21 with PCNA. Oncogene. 11:1931-1937.
7. Smith, M.L., Chen, I-T., Zhan, Q., O'Connor, P., Fornace, Jr., A.J. (1995). Involvement of p53-regulated gene products in repair of UV-type DNA damage. Oncogene. 10:1053-1059.
8. Smith, M.L., Chen, I-T., Zhan, Q., et al., (1994). Interaction of the p53-regulated protein gadd45 with PCNA. Science, 266, 1376-80.
9. Chen, I-T. and Chasin, L.A. (1994). Large exon size does not limit splicing. Mol. Cell Biol. 14:2140-46.