Integrative Life Sciences :
Developmental Regulation Network


Professor CHIBA Natsuko
Campus Seiryo campus
Laboratory Cancer Biology
Tel +81-22-717-8477
E-mail natsuko.chiba.c7@tohoku.ac.jp

I have been involved in clinical oncology in addition to basic research. Using this experience, I would like to contribute to the further understanding of carcinogenesis and to the development of novel cancer therapies.

March 1997 M.D. Tohoku University School of Medicine
March 1997 Ph.D. Tohoku University Graduate School of Medicine
April 1997-March 1998 Lecturer, Institute of Development, Aging and Cancer, Tohoku University
April 1998- March 1999 Medical Staff in Internal Medicine, Ishinomaki Red-Cross Hospital
April 1999- March 2002 Research Fellow in the laboratory of Dr. Jeffrey D. Parvin, Department of Pathology, Brigham and Women’s Hospital, Boston, U.S.A.
April 2002-July 2003 Medical Staff in Clinical Oncology, Tohoku University Hospital
August 2003-March 2007 Assistant Professor, Department of Clinical Oncology, Institute of Development, Aging and Cancer, Tohoku University
April 2007 Associate Professor, Department of Molecular Immunology, Institute of Development, Aging and Cancer, Tohoku University
April 2014-present Professor, Department of Cancer Biology, Institute of Development, Aging and Cancer, Tohoku University
Selected Publications
  1. Matsuzawa A, Kanno S, Nakayama M, Mochiduki H, Wei L, Shimaoka T, Furukawa Y, Kato K, Shibata S, Yasui A, Ishioka C, and Chiba N. The BRCA1/BARD1-interacting protein OLA1 functions in centrosome regulation. Molecular Cell, 53(1):101-104, 2014
  2. Kais Z, Chiba N, Ishioka C, Parvin J D. Functional differences among BRCA1 missense mutations in the control of centrosome duplication. Oncogene, 9;31(6):799-804, 2012
  3. Wei L, Lan L, Yasui A, Tanaka K, Saijo M, Matsuzawa A, Kashiwagi R, Maseki E, Hu Y, Parvin J D, Ishioka C and Chiba N. BRCA1 contributes to transcription-coupled repair of DNA damage through polyubiquitination and degradation of Cockayne syndrome B protein. Cancer Science 102(10):1840-7, 2011
  4. Ransburgh D*, Chiba N*, Toland A, and Parvin J D. (*co-first author) The effect of BRCA1 missense mutations on homology directed recombination. Cancer Research 70(3);988-95, 2010
  5. Wei L, Lan L, Hong Z, Yasui A, Ishioka C, and Chiba N. Rapid recruitment of BRCA1 to DNA double-strand breaks is dependent on its association with Ku80. Mol. Cell. Biol. 28(24); 7380-93, 2008
Activities in Academic Societies

The Molecular Biology Society of Japan, Japanese Cancer Association, Japan Society of Clinical Oncology, Japanese Society of Medical Oncology, Japan HBOC Consortium

Recent Activities

Germline mutations in the Breast cancer associated gene 1 (BRCA1) predispose women to breast and ovarian cancers. BRCA1 is involved in many cellular processes, including DNA repair and centrosome regulation. Defects in the regulatory mechanisms of centrosomes and DNA repair result in defective mitosis, chromosome segregation errors, and the accumulation of DNA damage. These are significant sources of genome instability, a hallmark of cancer.

Although the functions of BRCA1 in the DNA repair pathway have been extensively studied, the mechanism of centrosome regulation by BRCA1 is largely unknown. Recently, we identified a novel BRCA1-related protein, Obg-like ATPase 1 (OLA1), which functions in centrosome regulation together with BRCA1. The breast cancer-derived OLA1 mutation does not bind to BRCA1 and fails to rescue the OLA1 knockdown-induced centrosome amplification. The familial breast cancer-derived BRCA1 mutation I42V abrogates the binding of BRCA1 to OLA1. These findings suggest that OLA1 plays a role in centrosome duplication and functions as a tumor suppressor together with BRCA1.

To analyze the further functions of BRCA1 and its related proteins, we perform cytological analyses, analyses using genetically modified mice, and analyses of clinical specimens. These researches will contribute to the further understanding of carcinogenesis and to the development novel cancer therapies

Fig. 1 Centrosome amplification by knockdown of OLA1.
Fig. 2 Accumulation of BRCA1 at the sites of DNA damage.

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