Randall J. Ruch, Ph.D.
|Randall J. Ruch, Ph.D.
Associate Professor of Biochemistry & Cancer Biology
Cells communicate with each other in many ways using secreted molecules (e.g., hormones, cytokines, growth factors, and nitric oxide) and direct cell contact through cellular junctions (e.g., synapses, desmosomes, hemidesmosomes, adherens junctions, and gap junctions). Gap junctions are comprised of channels that link the interiors of neighboring cells and permit the diffusion of small molecules and ions directly between cells. This gap junctional intercellular communication (GJIC) facilitates homeostasis, signaling and coordination of cells, and the regulation of cell birth, death and differentiation. Gap junction defects cause some form of peripheral neuropathy, hereditary deafness, cardiac arrhythmia, cataracts, infertility, and skin disease, and are also involved in atherosclerosis, birth defects, and cancer. My current research interests are to understand how gap junctions become defective in cancer cells and carcinogen-treated cells, how gap junctions and their protein components known as connexins are regulated, and how gap junctions affect anti-cancer drug toxicity.
Member of the mentoring faculty for the Biomedical Sciences Graduate Program (Cancer Biology Track).
1978 B.S., Biology, Florida State University
1981 M.S., Zoology, The Ohio State University
1988 Ph.D., Pathology, Medical University of Ohio
1988-1990 Post-doc, Medical University of Ohio
1990-1992 Post-doc, Wayne State University
2006-pres. Assistant Dean for Admissions, Biomedical Graduate Programs, University of Toledo College of Medicine
2004-pres. Associate Professor, Dept. of Biochemistry and Cancer Biology, University of Toledo College of Medicine
2001-2006 Associate Dean for Graduate Student Recruitment, Medical University of Ohio
1999-2001 Director, Molecular Basis of Disease Ph.D. Graduate Program, Medical University of Ohio
1997-2004 Associate Professor, Dept. of Pathology, Medical College of Ohio
1996-1999 Vice-Director, Molecular Basis of Disease Ph.D. Graduate Program, Medical University of Ohio
1992-1997 Assistant Professor, Dept. of Pathology, Medical College of Ohio
PROFESSIONAL AFFILIATIONS & ACTIVITIES:
Ad Hoc Reviewer:
1992 National Institutes of Occupational Safety and Health
1993 International Human Frontier Science Program Organization
1994 Great Lakes Health Research Program
1995-96 National Institutes of Health, NIDDK, Program Project Reviewer
1996 National Institutes of Health, Chemical Pathology A Study Section
1997 National Institutes of Health, Alcohol and Toxicology II Study Section
1997 Medical Research Council of Canada
1997 Department of Energy
1999-2000 Veterans Administration
2001 National Cancer Institute of Canada
2001 Great Lakes Research Fund
2001-present Ohio Cancer Research Associates, Review Panel member
2002 Nebraska Research Initiative 2002
2003 Philip Morris External Research Program
Journal Peer Review:
Biochimica Biophysica Acta, Biomed Central - Cancer, Biotechniques, Brain Research, British Journal of Cancer, Cancer Chemotherapy & Pharmacology, Cancer Research, Carcinogenesis, Cell Biology and Toxicology, Cell Growth & Differentiation, Chemical Research in Toxicology, Clinical and Experimental Metastasis, Comparative Biochemistry and Physiology, Developmental Genetics, Digestion, Environmental Science and Technology, Environmental Toxicology & Chemistry, Experimental Cell Research, The FASEB Journal, Fundamental and Applied Toxicology, Histology and Histopathology, In Vitro Cellular & Developmental Biology, International Journal of Radiation Oncology, Biology, Physics, Journal of Agriculture and Food Chemistry, Journal of the American College of Toxicology, Journal of Cell Science, Journal of Clinical Investigation, Journal of Toxicology and Environmental Health, Life Sciences, Molecular Carcinogenesis, Molecular and Cellular Biochemistry, Molecular Medicine Today, Nature, Neuroscience, Nutrition and Cancer, The Ohio Journal of Science, Pesticide Biochemistry and Physiology, Radiation Research, Toxicological Sciences, Toxicology and Applied Pharmacology, Toxicon
Hanna EA, Umhauer S, Roshong SL, Piechocki MP, Fernstrom MJ, Fanning JD, and Ruch RJ (1999) Gap junctional intercellular communication and connexin43 expression in human ovarian surface epithelial cells and ovarian carcinomas in vivo and in vitro. Carcinogenesis 20:1369-1373.
Piechocki MP, Burk RD, and Ruch RJ (2000) Transcriptional regulation of connexin32 in rat liver cells. Biochim. Biophys. Acta 1491:107-122.
Koffler L, Park IK, Cesen-Cummings K, Thompson DC, Dwyer-Nield LC, Rice P, Mamay C, Malkinson AM, and Ruch RJ (2000) Growth inhibition in G1 and altered expression of cyclin D1 and p27kip-1 after forced connexin expression in lung and liver carcinoma cells. J. Cell. Biochem. 79:347-354.
Nielsen M, Ruch RJ, and Vang O (2000) Resveratrol restores tumor-promoter induced inhibition of gap junctional intercellular communication. Biochem. Biophys. Res. Commun. 275:804-809.
Ruch RJ, Porter S, Koffler LD, Dwyer-Nield LD, and Malkinson AM (2001) Defective gap junctional intercellular communication in lung cancer: loss of an important mediator of tissue homeostasis and phenotypic regulation. Exp. Lung Res. 27:231-243.
Ruch RJ, Trosko JE, and Madhukar BV (2001) Inhibition of gap junctions by TPA: Role of extracellular signal regulated kinases. J. Cell. Biochem. 83:163-169.
Fernstrom MJ, Koffler LD, Abou-Rjaily G, Boucher PD, Shewach DS, and Ruch RJ (2002) Neoplastic reversal of human ovarian carcinoma cells transfected with Connexin43. Exp. Mol. Pathol. 73:54-60.
Koffler LD, Fernstrom MA, Akiyama TE, Gonzalez FJ, and Ruch RJ (2002) Positive regulation of connexin32 transcription by hepatocyte nuclear factor-1a. Arch. Biochem. Biophys., 407:160-167.
Warner KA, Fernstrom, MF, and Ruch RJ (2003) Inhibition of mouse hepatocyte gap junctional intercellular communication by phenobarbital in vivo and in vitro correlates with strain-specific hepatocarcinogenesis. Toxicol. Sci., 70:190-197.
Peebles KA, Duncan MW, Ruch, RJ, and Malkinson AM (2003) Proteomic analysis of a mouse lung carcinoma cell line whose tumorigenicity has been abrogated by transfection with the gap junction structural gene for connexin43, Gja1. Carcinogenesis, 24:651-657.
Abou-Rjaily GA, Lee SJ, May D, Al-Share QY, DeAngelis AM, Ruch RJ, Neumaier M, Kalthoff H, Lin S-H and Najjar SM (2004) CEACAM1 links metabolism to epidermal growth factor receptor-dependent cell proliferation. A potential connection between obesity and cancer. J. Clin. Invest., 114: 944-952.
Gentry B, Im M, Boucher PD, Ruch RJ, Shewach DS (2005) GCV phosphates are transferred between HeLa cells despite lack of bystander cytotoxicity. Gene Therapy, 12:1033-1041.