◀ Back to TP53
BCL6 — TP53
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Vitale et al., Endocrinology 2000
(Necrosis) :
This type of apoptosis is
p53 independent, does not require protein synthesis, and is not
induced by modulation of Bcl-2,
Bcl-XL , or Bax protein expression
Takehara et al., Hepatology 2001
(Carcinoma, Hepatocellular...) :
Ectopic expression of transcriptionally active
p53 alone was not sufficient for the activation of apoptosis in p53-null Hep3B cells, but apoptosis was
induced when endogenous
Bcl-xL was simultaneously inhibited by antisense oligonucleotide in these cells
Raymond et al., FASEB J 2004
:
VSMC exposed to serum-free medium conditioned by apoptotic EC showed increased ERK 1/2 phosphorylation, enhanced
Bcl-xl expression, and
inhibition of
p53 expression
Phan et al., Nature 2004
:
BCL6 represses
p53 transcription by binding two specific DNA sites within the p53 promoter region and, accordingly, p53 expression is absent in germinal-centre B cells where BCL6 is highly expressed
Margalit et al., Blood 2006
(Lymphoma, B-Cell) :
BCL6 is
regulated by
p53 through a response element frequently disrupted in B-cell non-Hodgkin lymphoma ... The increase in
BCL6 mRNA levels was
attenuated by the
p53 inhibitor PFT-alpha
Sirach et al., Cell Death Differ 2007
(Carcinoma, Hepatocellular...) :
Finally, KLF6 silencing caused
p53 upregulation and
inhibited Bcl-xL expression, to induce cell death by apoptosis
Lee et al., Int J Cancer 2008
(Carcinoma, Squamous Cell...) :
Greater modulation among HNSCC lines expressing low wt p53 than those over expressing mt p53 protein suggested that decreased
p53 expression might
enhance activation of NF-kappaB, STAT3 and
BCL-XL
Cerchietti et al., Cancer Res 2008
(Lymphoma, Large B-Cell, Diffuse) :
We report that a specific inhibitor of
BCL6 called BPI can
trigger a
p53 response in DLBCL cells ... This was partially due to induction of p53 activity and partially due to relief of direct
repression by
BCL6 of
p53 target genes
Ranuncolo et al., J Biol Chem 2008
:
Although BCL6 can directly repress
TP53 in centroblasts,
BCL6 induced TP53 expression in primary fibroblasts and B-cells, and these cells underwent p53 dependent growth arrest and senescence in the presence of physiological levels of BCL6 ... Although
BCL6 can directly
repress TP53 in centroblasts, BCL6 induced TP53 expression in primary fibroblasts and B-cells, and these cells underwent p53 dependent growth arrest and senescence in the presence of physiological levels of BCL6
Zhou et al., Cell Mol Immunol 2009
:
Treatment of CpG DNA could reduce the expression of caspase 3, increase IAP and
Bcl-xL expressions, and
inhibit p53 protein expression which level was increased in B cell spontaneous apoptosis at 24 h. AKT kinase activity was increased with the incubation of CpG DNA
Lee et al., Chem Biol Interact 2011
:
TRAIL induced nuclear damage, decreased Bid, Bcl-2,
Bcl-xL and survivin protein levels,
increased Bax levels, induced cytochrome c release, activated caspases ( -8, -9 and -3 ) and increased
tumor suppressor p53 levels
Banu et al., Toxicol Appl Pharmacol 2011
:
Our data indicated that CrVI : ( i ) induced DNA fragmentation and increased apoptosis, ( ii ) increased cytochrome c release from the mitochondria to cytosol, ( iii ) downregulated anti-apoptotic Bcl-2,
Bcl-XL , HSP70 and HSP90 ; upregulated pro-apoptotic BAX and BAD, ( iv ) altered translocation of Bcl-2, Bcl-XL, BAX, BAD, HSP70 and HSP90 to the mitochondria, ( v ) upregulated p-ERK and p-JNK, and selectively translocated p-ERK to the mitochondria and nucleus, ( vi ) activated caspase-3 and PARP, and ( vii ) increased phosphorylation of
p53 at ser-6, ser-9, ser-15, ser-20, ser-37, ser-46 and ser-392,
increased p53 transcriptional activation, and downregulated MDM-2
Hurtz et al., J Exp Med 2011
(Disease Models, Animal...) :
BCL6 mediated repression of
p53 is critical for leukemia stem cell survival in chronic myeloid leukemia ...
BCL6 represses Arf and
p53 in CML cells and is required for colony formation and initiation of leukemia
Park et al., Mol Carcinog 2012
(Colonic Neoplasms...) :
HFD feeding increased tumor tissue levels of Ki67, cyclin A, cyclin D1, CDK2,
Bcl-xL , and Bcl-2 ; reduced
p53 levels and TUNEL positive apoptotic cells ;
increased the levels of CD45, CD68, CD31, VEGF, P-VEGF receptor-2, iNOS, and COX-2 as well as hemoglobin content ; and increased the levels of HIF-1a, P-STAT3-Y705, P-STAT3-S727, P-I?B-a, P-p65, p65, P-c-Jun, P-Akt, P-ERK1/2, P-p38, and P-SAPK/JNK
Li et al., Dalton Trans 2012
(Neoplasms) :
DNA damage subsequently activated
p53 phosphorylation and
inhibited the expression of
Bcl-xL , resulting in activation of caspase-3, -8 and -9, and cleavage of poly ( ADP-ribose ) polymerase ( PARP )
Swaminathan et al., Nat Med 2013
(Cell Transformation, Neoplastic...) :
After productive VH-DJH gene rearrangement, pre-B cell receptor signaling ends BACH2 mediated negative selection through
B cell lymphoma 6 (BCL6) mediated repression of
p53 ... Chromatin immunoprecipitation sequencing and gene expression analyses carried out by us revealed that BACH2 competes with BCL6 for promoter binding and reverses
BCL6 mediated repression of
p53 and other cell cycle checkpoint-control genes
Merchant et al., Oncogene 1996
:
These observations indicate that Bcl-2 and
Bcl-xL are regulated differently in
response to wild-type
p53 activity and that, while correction of mutant p53 phenotype may effectively kill cells having Bcl-2 as their major defense against PCD, this is not necessarily the case in cells using Bcl-xL as their primary defense