Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/92649
Title: TRANSGLUTAMINASE 2 CONTRIBUTES TO A P53-DEPENDENT AUTOPHAGY PROGRAM TO SUPPRESS ONCOGENIC TRANSFORMATION
Authors: YEO SHI YUN (YANG SHIYUN)
Keywords: TGM2, autophagy, oncogenic transformation, p53, p21, HMECs
Issue Date: 22-Jul-2014
Citation: YEO SHI YUN (YANG SHIYUN) (2014-07-22). TRANSGLUTAMINASE 2 CONTRIBUTES TO A P53-DEPENDENT AUTOPHAGY PROGRAM TO SUPPRESS ONCOGENIC TRANSFORMATION. ScholarBank@NUS Repository.
Abstract: THE TUMOR SUPPRESSOR GENE P53 PROTECTS CELLS FROM MALIGNANT TRANSFORMATION, AND OVER HALF OF ALL HUMAN TUMORS HAVE ACQUIRED MUTATIONS THAT INACTIVATE P53. HOWEVER TUMORS WITH WILD-TYPE P53 OFTEN ACCUMULATE OTHER ALTERATIONS WITHIN THE P53 SIGNALING PATHWAY TO PROMOTE TUMORIGENESIS. TO IDENTIFY NEW COMPONENTS OF THIS PATHWAY, WE PERFORMED A LOSS-OF-FUNCTION SCREEN FOR GENES WHOSE IMPAIRMENT DEBILITATE P53 FUNCTIONS AND ENABLED ONCOGENIC TRANSFORMATION OF HUMAN MAMMARY EPITHELIAL CELLS (HMECS) EXPRESSING HTERT, SV40 SMALL T ANTIGEN AND ONCOGENIC RASV12 IN THE PRESENCE OF WILD-TYPE P53. WE IDENTIFIED TRANSGLUTAMINASE 2 (TGM2) AS A PUTATIVE TUMOR SUPPRESSOR AND A NOVEL COMPONENT IN THE P53 PATHWAY. TGM2 SUPPRESSED COLONY FORMATION OF HMECS IN SOFT AGAR AND TUMOR FORMATION IN A XENOGRAFT MOUSE MODEL. THE DEPLETION OF GROWTH SUPPLEMENTS IN CELL CULTURE INDUCED BOTH TGM2 EXPRESSION AND AUTOPHAGY IN A P53-DEPENDENT MANNER, AND TGM2 PROMOTED AUTOPHAGIC FLUX BY ENHANCING AUTOLYSOSOME CLEARANCE.
URI: http://scholarbank.nus.edu.sg/handle/10635/92649
Appears in Collections:Ph.D Theses (Open)

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