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Mutated TP53 activates apoptotic process. 144 / 144
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144
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"This study was undertaken to dissect the molecular mechanism underlying sulindac induced apoptosis in human colon cancer cell line HT-29 (mutant p53), focusing on nuclear translocation of AIF, DFF and endonuclease G. On induction of apoptosis by sulindac, it was associated with decreased mitochondrial membrane potential, nuclear expression of active caspase-3, cleavage of poly (ADP-ribose) polymerase, translocation of mitochondrial proteins to the nucleus, and morphological evidence of nuclear condensation."
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"Reactivation of mutant p53 (mtp53) to a wild-type form using the small molecule " p53 reactivation and induction of massive apoptosis " (Prima-1) in nude mice bearing mtp53 human breast cell tumors restored the p53 directed apoptosis pathway and enhanced the exposure of PS in tumors."
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"Screening of the diversity set from the National Cancer Institute led to the discovery of some chemical chaperones with mutant p53 reactivating capacity : compound 854 known as PRIMA-1 (p53 reactivation and induction of massive apoptosis) and compound 954 known as MIRA-3 (mutant p53 dependent induction of rapid apoptosis)."
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"Indeed, based on crystallographic structural and computational analyses, PRIMA-1 (p53 reactivation and induction of massive apoptosis-1) and MIRA-3 (mutant p53 reactivation and induction of rapid apoptosis in vivo) were developed to convert mutant p53 and restore p53 function leading to effective activation of downstream apoptosis inducing targets, such as caspase-2, puma, and Bax [XREF_BIBR, XREF_BIBR]."
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"Our result suggests that mutant p53 in U373MG cells can induce apoptosis through a transcription independent pathway, as the level of cytochrome c increased in the cytosolic fraction, whereas the level of cytochrome c decreased in the mitochondrial fraction with a decrease in mitochondrial membrane potential (XREF_FIG)."
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"Our results suggest that increased DNA instability, enhanced proliferative activity, p53 mutation, and induction of DFF45 and VEGF may allow cancer cell proliferation, enhance their survival by escaping apoptosis, and provide abundant nutrients during early-stage carcinogenesis of oral leukoplakia."
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"Overexpression of Bcl-2 in the mammary gland using a whey acidic protein (WAP) promoter driven Bcl-2 transgene inhibits apoptosis in the mammary gland during pregnancy, lactation, and involution, and also counteracts apoptosis induced by overexpression of a mutant p53 transgene (WAP-p53 172 R-L)."
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"Similarly to MIRA-3 (mutant p53 reactivation and induction of rapid apoptosis), and STIMA-1 (SH group targeting and induction of massive apoptosis), which also rescue mutant p53 function via thiol modification within the DNA binding domain, PRIMA-1 increased p53 activity by restoring sequence specific DNA binding, and triggered the mitochondria dependent intrinsic apoptosis program via activation of caspase-2 [XREF_BIBR]."
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"These results indicated that the tumor growth inhibition of SNL-P administration might correlate with the reduction of TNF-alpha level of blood serum, which resulted in a massive necrosis in tumor tissues and the up-regulation of Bax and down-regulation of Bcl-2 and mutant p53 gene expression, which triggered apoptosis in tumor cells."
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"In this scenario, we previously demonstrated that the combination of ibrutinib with MDM2-inhibitors synergized in promoting apoptosis in B-CLL cell lines carrying wild-type p53 as well as 17p13 deletion and/or TP53 mutations [16], and that ibrutinib combined with gamma-secretase inhibitors exhibited enhanced cytotoxicity that was coupled with the down-regulation of the c-MYC oncogene [8]."
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"Also, knockin mice carrying a mutant p53 (p53 K117R; K161R; K162R) that can not induce cell cycle arrest, apoptosis, and senescence fail to develop tumors at an early age, unlike p53-null mice, likely because p53 K117R; K161R; K162R retains the abilities to regulate energy metabolism and reduce reactive oxygen species [XREF_BIBR]."
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"Enhancing endogenous ceramide by disrupting ceramide glycosylation sensitizes mutant p53 cells to drug induced apoptosis, even though it does not significantly alter p53 protein levels, as reported previously and detected by Western blotting in the present study (XREF_FIG, XREF_FIG, XREF_FIG, XREF_SUPPLEMENTARY)."
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"Apoptotic cell analysis showed that transfection of TP53 wild-type NUGC4 and TP53 mutant MKN7 with siRNA-TRIM37 increased early apoptosis (annexin V-positive and PI-negative) and late apoptosis (annexin V/PI-double positive), respectively, at 72 h post-transfection compared with transfection with control siRNA."