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The p53/p21 Complex Regulates Cancer Cell Invasion and Apoptosis by Targeting Bcl-2 Family Proteins

https://doi.org/10.1158/0008-5472.can-16-2098
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39/39 checkable references clean · checked 2026-07-23

Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.

1 without a DOI — not checked. A reference deposited without a DOI is never matched by title or guessed at; it stays outside the checked set, and this line discloses that.

The 39 checked references that resolve
resolves10.1083/jcb.201009059
p53 and its mutants in tumor cell migration and invasion
resolves10.1038/nrc2657
p21 in cancer: intricate networks and multiple activities
resolves10.15252/embr.201438587
Cooperative actions of p21WAF1 and p53 induce Slug protein degradation and suppress cell invasion
resolves10.1016/j.bbabio.2008.10.005
The mitochondrial p53 pathway
resolves10.1038/nrm3722
Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy
resolves10.18632/oncotarget.6405
Bcl-2 family proteins as regulators of cancer cell invasion and metastasis: a review focusing on mitochondrial respiration and reactive oxygen species
resolves10.18632/oncotarget.2320
Nuclear and cytoplasmic p53 suppress cell invasion by inhibiting respiratory Complex-I activity via Bcl-2 family proteins
resolves10.1016/j.cellsig.2012.01.019
Bcl-w promotes cell invasion by blocking the invasion-suppressing action of Bax
resolves10.1073/pnas.92.10.4407
Wild-type p53 protein undergoes cytoplasmic sequestration in undifferentiated neuroblastomas but not in differentiated tumors.
resolves10.1093/neuonc/4.3.171
Cytoplasmic localization of wild-type p53 in glioblastomas correlates with expression of vimentin and glial fibrillary acidic protein
resolves10.1158/0008-5472.CAN-05-4254
Bcl-w Promotes Gastric Cancer Cell Invasion by Inducing Matrix Metalloproteinase-2 Expression via Phosphoinositide 3-Kinase, Akt, and Sp1
resolves10.4049/jimmunol.156.9.3469
Fas mediates apoptosis in human monocytes by a reactive oxygen intermediate dependent pathway
resolves10.1038/sj.onc.1208836
Mitochondrial localization of p53 during adenovirus infection and regulation of its activity by E1B-19K
resolves10.1186/1748-717X-7-153
Establishment of animal model for the analysis of cancer cell metastasis during radiotherapy
resolves10.1182/blood.V98.2.414
Apaf-1 protein deficiency confers resistance to cytochromec–dependent apoptosis in human leukemic cells
resolves10.1074/jbc.M507611200
WT p53, but Not Tumor-derived Mutants, Bind to Bcl2 via the DNA Binding Domain and Induce Mitochondrial Permeabilization
resolves10.1182/blood-2007-02-072082
Mutations in the DNA-binding codons of TP53, which are associated with decreased expression of TRAILreceptor-2, predict for poor survival in diffuse large B-cell lymphoma
resolves10.3904/kjim.2003.18.2.98
Prognostic Significance of p21 and p53 Expression in Gastric Cancer
resolves10.1200/JCO.2002.09.147
Clinical Significance of p21 Expression in Non–Small-Cell Lung Cancer
resolves10.1038/ncb2641
p53 mutations in cancer
resolves10.18632/oncotarget.9770
Mutation spectrum of TP53 gene predicts clinicopathological features and survival of gastric cancer
resolves10.18632/oncotarget.4080
Survival of patients with structurally-grouped<i>TP53</i>mutations in ovarian and breast cancers
resolves10.1101/cshperspect.a008722
Multiple Functions of BCL-2 Family Proteins
resolves10.1016/j.cell.2005.07.002
Bcl-2 Antiapoptotic Proteins Inhibit Beclin 1-Dependent Autophagy
resolves10.1038/ncb1192
Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes
resolves10.4161/auto.6260
Bcl-2 family members: Dual regulators of apoptosis and autophagy
resolves10.1042/bj20030868
Bcl-2 activates a programme of premature senescence in human carcinoma cells
resolves10.1016/S0006-291X(03)00402-9
Bcl-2 promotes premature senescence induced by oncogenic Ras
resolves10.1074/jbc.M305015200
Bcl-xL and E1B-19K Proteins Inhibit p53-induced Irreversible Growth Arrest and Senescence by Preventing Reactive Oxygen Species-dependent p38 Activation
resolves10.1158/1541-7786.MCR-09-0354
Bcl-2 Overexpression Induces a Partial Epithelial to Mesenchymal Transition and Promotes Squamous Carcinoma Cell Invasion and Metastasis
resolves10.1111/j.1349-7006.2010.01552.x
Bcl‐X <sub>L</sub> and STAT3 mediate malignant actions of γ‐irradiation in lung cancer cells
resolves10.1002/hep.24543
Promotion of tumor cell metastasis and vasculogenic mimicry by way of transcription coactivation by Bcl-2 and Twist1: A study of hepatocellular carcinoma
resolves10.1186/s12885-015-1485-5
Constitutive expression of Bcl-2 induces epithelial-Mesenchymal transition in mammary epithelial cells
resolves10.3727/096504012X13473664562628
Quinacrine-Mediated Autophagy and Apoptosis in Colon Cancer Cells Is Through a p53- and p21-Dependent Mechanism
resolves10.1016/j.canlet.2015.04.014
p53-mediated autophagic regulation: A prospective strategy for cancer therapy
resolves10.1371/journal.pone.0066464
PUMA Cooperates with p21 to Regulate Mammary Epithelial Morphogenesis and Epithelial-To-Mesenchymal Transition
resolves10.1038/cddis.2015.44
Reactive oxygen species and p21Waf1/Cip1 are both essential for p53-mediated senescence of head and neck cancer cells
resolves10.1016/j.febslet.2014.07.009
Phospholipase D2 downregulation induces cellular senescence through a reactive oxygen species–p53–p21<sup>Cip1/WAF1</sup> pathway
resolves10.1126/science.282.5393.1497
Requirement for p53 and p21 to Sustain G <sub>2</sub> Arrest After DNA Damage
The 1 reference without a DOI — listed, not checked
no DOI — not checkedExpression of p53 and p21 and the clinical response for hyperthermochemoradiotherapy in patients with squamous cell carcinoma of the esophagus
What this badge says. CiteStamped means the CHECKABLE references of this work were clean at the dated check: each resolved to a known work in a public registry, and none carried a retraction notice at that time. It says nothing about the quality, findings, or importance of the work itself, and nothing about references deposited without a DOI.

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