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陳一村

l Title: Associate  Professor

l Address:

       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.)

l Phone: 02-2826-7213 (Office)
       02-2826-7000 ext. 5826 (Lab)

l E-mail: chenit@ym.edu.tw

 

l Educational Background:

Kansas State Univ.

Post Doctor training: Columbia Univ. & NIH

 

l Specialty:

       Molecular Biology, Cancer Biology, Cell Signal Transduction & Gene Regulation

 

l 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.

 

l Current Projects

         In cancers without p53 mutations, the p53 function is often inactivated by MDM2, a negative regulator of p53. Many stress signals can disrupt the MDM2-p53 feedback loop. One of the new stressors is so-called nucleolar stress or “ribosomal stress” and results from disruption of ribosome biogenesis. In response to ribosomal stress, several ribosomal proteins (RPs) including L11, L23, L5, and S7, are released from nucleolus and bind to MDM2. These RPs-MDM2 interactions inhibit MDM2-mediated p53 degradation, thereby activates p53-dependent cell cycle arrest or apoptosis. Recently, we have tested this model in wt p53 lung cancer cell line, and we showed that Ling-Zhi 8, a protein from Ling-Zhi, exhibited antitumor activity via RP-MDM2-p53 pathway (Wu et al., 2011).

Following up this concept, we are investigating the role of metformin, an anti-diabetic drug, in reducing cancer risk in diabetic patients. Among other effects of metformin against cancer cell proliferation, we believe that metformin also activate RP-MDM2-p53 pathway, where we have found another ribosomal protein L7 that might participate in this pathway.

In addition, we are interesting in studying DNA repair of double strands breaks induced by IR, chemo-drugs which are often occurred in cancer therapy. Some families have high risk of getting breast cancer due to inherited mutation of breast cancer genes (e.g. Braca1), which lack in homologous recombination repair. These breast cancer cells are sensitive to a drug that blocking another repair pathway, so called “synthetic lethal” approach. Another example is ATM-p53 pathway, we are testing this model.

 

l Selected Publications

Ø Wu, CT, et al, Ling Zhi-8 mediates p53-dependent growth arrest of lung cancer cells proliferation via the ribosomal protein S7-MDM2-p53 pathway. Carcinogenesis, 32:12 (1890-1896) 2011. (Corresponding)

Ø Schu-Rern Chern, Sheng-Hsiang Li, Chung-Hao Lu and Edmund IT Chen*. Spatiotemporal expression of the serine protease inhibitor, SERPINE2, in the mouse placenta and uterus during the estrous cycle, pregnancy, and lactation. Reproductive Biology and Endocrinology 2010, 8:127 -141.

Ø 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.

Ø 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.

Ø 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.

Ø 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.

Ø 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.

Ø 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.

Ø 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.

Ø Smith, M.L., Chen, I-T., Zhan, Q., et al., (1994). Interaction of the p53-regulated protein gadd45 with PCNA. Science, 266, 1376-80.

Ø Chen, I-T. and Chasin, L.A. (1994). Large exon size does not limit splicing. Mol. Cell Biol. 14:2140-46.