Please use this identifier to cite or link to this item: https://doi.org/10.7554/eLife.07101
Title: Transglutaminase 2 contributes to a TP53- induced autophagy program to prevent oncogenic transformation
Authors: Yeo S.Y.
Itahana Y. 
Guo A.K. 
Han R. 
Iwamoto K. 
Nguyen H.T.
Bao Y. 
Kleiber K. 
Wu Y.J. 
Bay B.H. 
Voorhoeve M. 
Itahana K. 
Issue Date: 2016
Publisher: eLife Sciences Publications Ltd
Citation: Yeo S.Y., Itahana Y., Guo A.K., Han R., Iwamoto K., Nguyen H.T., Bao Y., Kleiber K., Wu Y.J., Bay B.H., Voorhoeve M., Itahana K. (2016). Transglutaminase 2 contributes to a TP53- induced autophagy program to prevent oncogenic transformation. eLife 5 (Mar-16) : e07101. ScholarBank@NUS Repository. https://doi.org/10.7554/eLife.07101
Abstract: Genetic alterations which impair the function of the TP53 signaling pathway in TP53 wild-type human tumors remain elusive. To identify new components of this pathway, we performed a screen for genes whose loss-of-function debilitated TP53 signaling and enabled oncogenic transformation of human mammary epithelial cells. We identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway. TGM2 suppressed colony formation in soft agar and tumor formation in a xenograft mouse model. The depletion of growth supplements induced both TGM2 expression and autophagy in a TP53-dependent manner, and TGM2 promoted autophagic flux by enhancing autophagic protein degradation and autolysosome clearance. Reduced expression of both CDKN1A, which regulates the cell cycle downstream of TP53, and TGM2 synergized to promote oncogenic transformation. Our findings suggest that TGM2- mediated autophagy and CDKN1A-mediated cell cycle arrest are two important barriers in the TP53 pathway that prevent oncogenic transformation. � Yeo et al.
Source Title: eLife
URI: https://scholarbank.nus.edu.sg/handle/10635/163990
ISSN: 2050084X
DOI: 10.7554/eLife.07101
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