PMID- 22874565
OWN - NLM
STAT- MEDLINE
DCOM- 20130710
LR  - 20211021
IS  - 1554-8635 (Electronic)
IS  - 1554-8627 (Print)
IS  - 1554-8627 (Linking)
VI  - 8
IP  - 11
DP  - 2012 Nov
TI  - DEDD, a novel tumor repressor, reverses epithelial-mesenchymal transition by 
      activating selective autophagy.
PG  - 1675-6
LID - 10.4161/auto.21438 [doi]
AB  - Metastasis is the spread of cancer cells from their primary location to other 
      parts of the body. Metastatic cancer is responsible for most cancer deaths. 
      Increasing evidence indicates that epithelial-mesenchymal transition (EMT), a 
      crucial developmental program, contributes to control cancer invasion and 
      metastasis. We recently reported that death effector domain-containing 
      DNA-binding protein (DEDD), a key effector molecule for cell death signaling 
      receptors, attenuates EMT and acts as an endogenous suppressor of tumor growth 
      and metastasis. We found that DEDD physically interacts with the class III PtdIns 
      3-kinase complex containing PIK3C3 and BECN1, which controls critical aspects of 
      autophagy; this interaction activates autophagy and induces the 
      autophagy-mediated lysosomal degradation of SNAI/Snail and TWIST, two master 
      inducers of the EMT process. Further study reveals that the DEDD-PIK3C3 
      interaction can support the stability of PIK3C3 to maintain autophagic activity 
      and promote the degradation of SNAI and TWIST. Our finding indicates that DEDD is 
      a prognostic marker and a potential therapeutic target for the prevention and 
      treatment of cancer metastasis. Moreover, regulation of the DEDD-PIK3C3 
      interaction may serve as an entry point to translate modifiers of this 
      interaction into clinical endpoints.
FAU - Lv, Qi
AU  - Lv Q
AD  - Molecular Immunology and Pharmacology Group, State Key Laboratory of Bioactive 
      Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese 
      Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
FAU - Hua, Fang
AU  - Hua F
FAU - Hu, Zhuo-Wei
AU  - Hu ZW
LA  - eng
PT  - Journal Article
DEP - 20120809
PL  - United States
TA  - Autophagy
JT  - Autophagy
JID - 101265188
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Suppressor Proteins)
SB  - IM
CON - Lv Q, Wang W, Xue J, Hua F, Mu R, Lin H, Yan J, Lv X, Chen X, Hu ZW. DEDD 
      Interacts with PI3KC3 to Activate Autophagy and Attenuate Epithelial-Mesenchymal 
      Transition in Human Breast Cancer. Cancer Res. 2012;72:3238-50. PMID: 22719072
MH  - *Autophagy
MH  - DNA-Binding Proteins/*metabolism
MH  - *Epithelial-Mesenchymal Transition
MH  - Humans
MH  - Lysosomes/metabolism
MH  - Models, Biological
MH  - Proteolysis
MH  - Transcription Factors/metabolism
MH  - Tumor Suppressor Proteins/*metabolism
PMC - PMC3494596
OTO - NOTNLM
OT  - BECN1
OT  - DEDD
OT  - EMT
OT  - PIK3C3
OT  - SQSTM1
OT  - metastasis
OT  - protein interaction
OT  - selective autophagy
OT  - tumor growth
OT  - tumor stem cells
EDAT- 2012/08/10 06:00
MHDA- 2013/07/11 06:00
PMCR- 2013/11/01
CRDT- 2012/08/10 06:00
PHST- 2012/08/10 06:00 [entrez]
PHST- 2012/08/10 06:00 [pubmed]
PHST- 2013/07/11 06:00 [medline]
PHST- 2013/11/01 00:00 [pmc-release]
AID - 21438 [pii]
AID - 2012AUTO0280R [pii]
AID - 10.4161/auto.21438 [doi]
PST - ppublish
SO  - Autophagy. 2012 Nov;8(11):1675-6. doi: 10.4161/auto.21438. Epub 2012 Aug 9.