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Shioko  Kimura, Ph.D.

Shioko Kimura, Ph.D.

  • Center for Cancer Research
  • National Cancer Institute
Cancer Innovation Laboratory

RESEARCH SUMMARY

Dr. Kimura’s research focuses on understanding the role of homeodomain transcription factor NKX2-1, a marker for lung adenocarcinoma in humans, and its downstream target, a novel cytokine, secretoglobin (SCGB) 3A2, in development, homeostasis, physiology, and pathogenesis of diseases, particularly cancers of the thyroid and lung. Dr. Kimura uses cell culture and mouse models, and various genetically engineered mouse lines to investigate these problems. Her recent studies have suggested that SCGB3A2 has anti-cancer activity, and her group is currently extensively involved in uncovering the mechanism.

Areas of Expertise

1) NKX2-1, 2) SCGB3A2, 3) thyroid and lung carcinogenesis, 4) mouse model, 5) genetically engineered mice

Publications

Selected Recent Publications

A novel pathway of LPS uptake through syndecan-1 leading to pyroptotic cell death

Yokoyama S, Cai Y, Murata M, Tomita T, Yoneda M, Xu L, Pilon AL, Cachau RE, Kimura S.
Elife. 7: e37854, 2018. [ Journal Article ]

An in vivo model for thyroid regeneration and folliculogenesis

Iwadate M, Takizawa Y, Shirai YT, Kimura S.
Lab Invest. 98(9): 1126-1132, 2018. [ Journal Article ]

Secretoglobin superfamily protein SCGB3A2 deficiency potentiates ovalbumin-induced allergic pulmonary inflammation

Kido T, Yoneda M, Cai Y, Matsubara T, Ward JM, Kimura S.
Mediators Inflamm. Article ID 216465, 2014. [ Journal Article ]

Preclinical evaluation of human secretoglobin 3A2 in mouse models of lung development and fibrosis

Cai Y, Winn ME, Zehmer JK, Gillette WK, Lubkowski JT, Pilon AL, Kimura S.
Am J Physiol Lung Cell Mol Physiol. 306: L10-L22, 2014. [ Journal Article ]

Nkx2-1 represses a latent gastric differentiation program in lung adenocarcinoma

Snyder EL, Watanabe H, Magendantz M, Hoersch S, Chen TA, Wang DG, Crowley D, Whittaker CA, Meyerson M, Kimura S, Jacks T.
Mol Cell. 50(2): 185-99, 2013. [ Journal Article ]

Job Vacancies

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Team

Postbaccalaureate Fellow (CRTA)
Richard Clayton
Postdoctoral Fellow (Visiting)
Henrique Dias, Ph.D.
Postdoctoral Fellow (Visiting)
Shun Nakayama, Ph.D.
Research Fellow
Yo-Taro Shirai, Ph.D.

Covers

Journal of Cancer - October 2016

Co-expression of Achaete-Scute Homologue-I and Calcitonin Gene-Related Peptide during NNK-Induced Pulmonary Neuroendocrine Hyperplasia and Carcinogenesis in Hamsters

Published Date

Cover:  Co-expression of Achaete-Scute Homologue-I and Calcitonin Gene-Related Peptide during NNK-Induced Pulmonary Neuroendocrine Hyperplasia and Carcinogenesis in Hamsters

Abstract:  Achaete-scute homologue-1 or ASCL1 (MASH1, hASH1) plays roles in neural development and pulmonary neuroendocrine (NE) differentiation, and it is expressed in certain lung cancers. This study was aimed to assess whether and/or how ASCL1 plays a role in 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced pulmonary NE hyperplasia and carcinogenesis in hamsters. Hamsters were injected 3 times weekly with either NNK or solvent alone (control) for treatment periods of 6 and 24 weeks, both without and with 6-week recovery. Immunohistochemical analysis was carried out to examine the expressions of ASCL1, CGRP (calcitonin gene-related peptide), secretoglobin SCGB1A1 (club [Clara] cell specific 10 kD protein, CC10, CCSP), synaptophysin (SYP), and PCNA (proliferating cell nuclear antigen). The number of ASCL1-expressing NE foci per airway increased from 0.8 in controls to 1.6 and 2.0 during NNK exposure for 6 and 24 weeks, respectively, and the number of cells per foci doubled after NNK exposure. Most ASCL1-expressing cells in NEBs (neuroepithelial bodies) were also CGRP immunoreactive; NNK enhanced this co-expression with CGRP, a NE marker with known proliferation-promoting properties. NNK also increased PCNA expression within NE foci. NNK-induced tumors showed no immunoreactivity for NE markers. This study confirms ASCL1 as an excellent marker for pulmonary NE cells and demonstrates CGRP co-expression in ASCL1-positive NEB cells participating in NNK-induced NE hyperplasia.