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Glucose deprivation triggers protein kinase C-dependent β-catenin proteasomal degradation

Authors
 Seung-Won Choi  ;  Jun-Kyu Song  ;  Ye-Seal Yim  ;  Ho-Geun Yun  ;  Kyung-Hee Chun 
Citation
 Journal of Biological Chemistry, Vol.290(15) : 9863-9873, 2015 
Journal Title
 Journal of Biological Chemistry 
ISSN
 0021-9258 
Issue Date
2015
Abstract
Autophagy is a conserved process that contributes to cell homeostasis. It is well known that induction mainly occurs in response to nutrient starvation, such as starvation of amino acids and insulin, and its mechanisms have been extensively characterized. However, the mechanisms behind cellular glucose deprivation-induced autophagy are as of now poorly understood. In the present study, we determined a mechanism by which glucose deprivation induced the PKC-dependent proteasomal degradation of β-catenin, leading to autophagy. Glucose deprivation was shown to cause a sub-G1 transition and enhancement of the LC3-II protein levels, whereas β-catenin protein underwent degradation in a proteasome-dependent manner. Moreover, the inhibition of GSK3β was unable to abolish the glucose deprivation-mediated β-catenin degradation or up-regulation of LC3-II protein levels, which suggested GSK3β-independent protein degradation. Intriguingly, the inhibition of PKCα using a pharmacological inhibitor and transfection of siRNA for PKCα was observed to effectively block glucose deprivation-induced β-catenin degradation as well as the increase in LC3-II levels and the accumulation of a sub-G1 population. Together, our results demonstrated a molecular mechanism by which glucose deprivation can induce the GSK3β-independent protein degradation of β-catenin, leading to autophagy.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/141331
DOI
10.1074/jbc.M114.606756
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실)
Yonsei Authors
윤호근(Yoon, Ho Geun) ; 전경희(Chun, Kyung Hee)
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