PMID- 21447800
OWN - NLM
STAT- MEDLINE
DCOM- 20110718
LR  - 20191210
IS  - 1937-9145 (Electronic)
IS  - 1945-0877 (Linking)
VI  - 4
IP  - 166
DP  - 2011 Mar 29
TI  - c-MYC suppresses BIN1 to release poly(ADP-ribose) polymerase 1: a mechanism by 
      which cancer cells acquire cisplatin resistance.
PG  - ra19
LID - 10.1126/scisignal.2001556 [doi]
AB  - Cancer cells acquire resistance to DNA-damaging therapeutic agents, such as 
      cisplatin, but the genetic mechanisms through which this occurs remain unclear. 
      We show that the c-MYC oncoprotein increases cisplatin resistance by decreasing 
      production of the c-MYC inhibitor BIN1 (bridging integrator 1). The sensitivity 
      of cancer cells to cisplatin depended on BIN1 abundance, regardless of the p53 
      gene status. BIN1 bound to the automodification domain of and suppressed the 
      catalytic activity of poly(ADP-ribose) polymerase 1 (PARP1, EC 2.4.2.30), an 
      enzyme essential for DNA repair, thereby reducing the stability of the genome. 
      The inhibition of PARP1 activity was sufficient for BIN1 to suppress 
      c-MYC-mediated transactivation, the G(2)-M transition, and cisplatin resistance. 
      Conversely, overexpressed c-MYC repressed BIN1 expression by blocking its 
      activation by the MYC-interacting zinc finger transcription factor 1 (MIZ1) and 
      thereby released PARP1 activity. Thus, a c-MYC-mediated positive feedback loop 
      may contribute to cancer cell resistance to cisplatin.
FAU - Pyndiah, Slovenie
AU  - Pyndiah S
AD  - Molecular Signaling Program, Stanley S. Scott Cancer Center, Louisiana State 
      University Health Sciences Center, New Orleans, LA 70112, USA.
FAU - Tanida, Satoshi
AU  - Tanida S
FAU - Ahmed, Kazi M
AU  - Ahmed KM
FAU - Cassimere, Erica K
AU  - Cassimere EK
FAU - Choe, Chungyoul
AU  - Choe C
FAU - Sakamuro, Daitoku
AU  - Sakamuro D
LA  - eng
GR  - 1F31CA110205-01/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20110329
PL  - United States
TA  - Sci Signal
JT  - Science signaling
JID - 101465400
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Antineoplastic Agents)
RN  - 0 (BIN1 protein, human)
RN  - 0 (Bin1 protein, mouse)
RN  - 0 (MYC protein, human)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (PIAS2 protein, human)
RN  - 0 (Protein Inhibitors of Activated STAT)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 2.3.2.27 (Miz1 protein, mouse)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.4.2.30 (PARP1 protein, human)
RN  - EC 2.4.2.30 (Parp1 protein, mouse)
RN  - EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1)
RN  - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/genetics/*metabolism
MH  - Animals
MH  - Antineoplastic Agents/*pharmacology
MH  - Cell Division/drug effects/genetics
MH  - Cell Line, Tumor
MH  - Cisplatin/*pharmacology
MH  - DNA Damage/genetics
MH  - DNA Repair/drug effects/genetics
MH  - Drug Resistance, Neoplasm/*drug effects/genetics
MH  - G2 Phase/drug effects/genetics
MH  - Gene Expression Regulation, Neoplastic/drug effects/genetics
MH  - Humans
MH  - Mice
MH  - Neoplasms/drug therapy/genetics/*metabolism
MH  - Nerve Tissue Proteins/genetics/*metabolism
MH  - Nuclear Proteins/genetics/*metabolism
MH  - Poly (ADP-Ribose) Polymerase-1
MH  - Poly(ADP-ribose) Polymerases/genetics/*metabolism
MH  - Protein Inhibitors of Activated STAT/genetics/metabolism
MH  - Proto-Oncogene Proteins c-myc/genetics/*metabolism
MH  - Transcriptional Activation/drug effects/genetics
MH  - Tumor Suppressor Proteins/genetics/*metabolism
MH  - Ubiquitin-Protein Ligases
EDAT- 2011/03/31 06:00
MHDA- 2011/07/19 06:00
CRDT- 2011/03/31 06:00
PHST- 2011/03/31 06:00 [entrez]
PHST- 2011/03/31 06:00 [pubmed]
PHST- 2011/07/19 06:00 [medline]
AID - 4/166/ra19 [pii]
AID - 10.1126/scisignal.2001556 [doi]
PST - epublish
SO  - Sci Signal. 2011 Mar 29;4(166):ra19. doi: 10.1126/scisignal.2001556.