Bekir Cinar, Ph.D.

Research Scientist, Cancer Institute
Email:bekir.cinar@cshs.org
Phone:(310) 423-8658
Fax:(310) 423-8543

Institute Affiliation

Cancer Institute

Academic Appointments

Assistant Professor, Medicine
Assistant Professor, Biomedical Sciences

Awards and Activities

Edwin Beer Fellowship,The New York Academy of Medicine2010
Travel Grant Award, The Endocrine Society2006
Scholar-in-Training Award, American Association for Cancer Research Foundation2006
Associate Member, American Association for Cancer Research (AACR)2003
Society for Basic Urologic Research (SBUR)2003
The Endocrine Society2003 - 2010
American Association for Biochemistry and Molecular Biology (ASBMB)2012

Research Focus

Molecular and cellular basis of cancer promotion, metastatic progression, treatment resistance in disease models, particularly prostate and lung cancers. My laboratory employe tissue culture, animal models including transgenics and utilizes genetics, bioinformatics, and imaging modalities to address these issues. Our long term goal is to improve the current approach of cancer therapeutic strategies.

Research Contributions

Discovered a cross-talk between Hippo, AR, PI3-Kinase-AKT and mTOR signaling in cancer, particularly prostate cancer, showed Hippo/MST1/2 Ser-Thr protein kinase as an important link AR and PI3-Kinase-AKT-mTOR signaling in prostate cancer cells.

Current investigations include:

Signal transduction and gene expression in cancer and cancer stem cell evolution. Mechanisms of tumor promotion, metastatic progression, and treatment resistance. Tissue culture and animal model development.

Selected Publications

  1. Collak FK, Yagiz K, Luthringer DJ, Erkaya B, Cinar B: Threonine-120 phosphorylation regulated by phosphoinositide-3-kinase/Akt and mammalian target of rapamycin pathway signaling limits the antitumor activity of mammalian sterile 20-like kinase 1. The Journal of biological chemistry, 287(28): 23698-709, 2012
  2. Cinar B, Collak FK, Lopez D, Akgul S, Mukhopadhyay NK, Kilicarslan M, Gioeli DG, Freeman MR: MST1 is a multifunctional caspase-independent inhibitor of androgenic signaling. Cancer Res., 71(12): 4303-13, 2011
  3. Cinar B, Fang PK, Lutchman M, Di Vizio D, Adam RM, Pavlova N, Rubin MA, Yelick PC, Freeman MR: The pro-apoptotic kinase Mst1 and its caspase cleavage products are direct inhibitors of Akt1. EMBO J., 26(21): 4523-34, 2007
  4. Cinar B, De Benedetti A, Freeman MR: Post-transcriptional regulation of the androgen receptor by Mammalian target of rapamycin. Cancer Res., 65(7): 2547-53, 2005
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