Cisplatin p53

Author: mgrf

August undefined, 2024

WebDec 14, 2024 · Sensory neurotoxicity is a major, dose-limiting side effect of cisplatin, and recovery from CDDP-induced neuropathy is often incomplete; persisting in up to 55% of patients, even years after the... WebFeb 28, 2024 · Both complexes downregulate p53, except in U138-MG upon treatment with 28, and BCL-2 is downregulated by both complexes in all cells. In U87-MG, cisplatin upregulates PUMA, BAX, and NOXA. However, 28 upregulates NOXA in a more significant way, though BAX is downregulated, whereas PUMA levels remain unaltered.

p53-dependent global nucleotide excision repair of cisplatin-in…

WebJan 1, 2024 · The p53 and p21 proteins, which are senescence modulators, were upregulated at 48 h after cisplatin treatment ( Fig. 1 E and F). The mRNA levels of senescence-associated secretory phenotype (SASP) factors including interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α were increased in NRK cells at 48 h after … WebFeb 24, 2003 · Because p53 is induced by cisplatin in HCT116 cells (Fig. 1), it could have accounted for this apoptosis response. Transfection with PMS2 did not increase the apoptosis response to cisplatin. In p73-transfected cells, cisplatin did not stimulate apoptosis caused by the overexpression of p73. This is consistent with the inability of … hild wolfgang

Frontiers PRIMA-1 inhibits Y220C p53 amyloid …

WebActivation and involvement of p53 in cisplatin-induced nephrotoxicity. Cisplatin, a widely used chemotherapy drug, induces acute kidney injury, which limits its use and efficacy in … National Center for Biotechnology Information WebWe also demonstrate that the combination of PRIMA-1 and cisplatin is a promising approach for HCC therapy. Taken together, our data support the premise that targeting … WebOct 9, 2024 · However, the cisplatin resistance of cells associated with p53 and RAS status was quite different because the inhibition of STAT3 without regard of RAS V12 reduced the IC50 of cells to cispaltin ... smalltown america

The cardioprotective effect of human glucagon-like peptide-1

ATR-Chk2 signaling in p53 activation and DNA damage response ... - PubMed

WebIn the groups treated with magnolol and/or cisplatin, we found a significant increase in p53 and p21 expression. The p53 tumor suppressor gene is a critical transcription factor that controls angiogenesis, cell cycle, and DNA repair gene expression [ 44 ]. WebSep 24, 2024 · Cisplatin (CDDP) is the drug of choice against different types of cancer. However, tumor cells can acquire resistance to the damage caused by cisplatin, … hild wineryWebFeb 10, 2024 · Cisplatin, a broad-spectrum anti-tumor chemotherapeutic agent, is used in clinical practice for the treatment of various types of tumors 1, including hepatocellular carcinoma (HCC) and cervical... hild wine

"WebJul 31, 2014 · To confirm that p53 acted as a mediator of cisplatin-induced nephrotoxicity, we first assessed renal tubular damage by histology scores following 3 days of cisplatin administration in p53-null mice (p53 −/−). C57BL/6 mice, the most commonly used strain for p53 knockout, are relatively resistant to cisplatin-induced nephrotoxicity compared ... " - Cisplatin p53

Cisplatin p53

BCAT1 decreases the sensitivity of cancer cells to cisplatin by ...

WebIn human cells, the nucleotide excision repair (NER) process removes the intrastrand cross links from the genome, the efficiency of which is likely to be an important determinant of … WebMay 16, 2007 · Cisplatin induces p53 mitochondrial translocation: Effect of pifithrin-α. HCT116 wt cells (pre-treated or not with 10 μM pifithrin-α for 16 h) were treated with 50 μM cisplatin for 30 min or maintained untreated. Then, mitochondrial and cytosolic ( A) or total cell extracts ( B) were obtained.

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Webω-3 PUFAs regulated p53-mediated apoptosis, leading to protection of BM cells from apoptosis/cell cycle arrest induced by cisplatin. • ω-3 PUFAs inhibited cisplatin-induced oxidative damage in BM cells via activation of the NRF2-MDM2 pathway. Abstract Cisplatin is a chemotherapy medication used to treat a wide range of cancers. WebNational Center for Biotechnology Information

Webp53 mediates cisplatin-induced apoptosis in renal proximal tubular cells, and p53 can activate caspase-3 . Related to this, Li et al. described that HRPTEp cells treated with … WebDec 1, 2004 · Tubular damage by cisplatin leads to acute renal failure, which limits its use in cancer therapy. In tubular cells, a primary target for cisplatin is presumably the genomic DNA. However, the pathwa... Role …

WebMay 26, 1998 · Cisplatin treatment of teratocarcinoma cells with a wild-type p53 gene resulted in accumulation of the p53 protein through posttranscriptional mechanisms; induction of p53-target genes was also observed. Drug treatment resulted in rapid apoptosis in p53-wild-type cells but not in p53 −/− teratocarcinoma cells. WebMar 7, 2008 · Recent work has suggested a role for p53 in cisplatin-induced renal cell apoptosis and kidney injury; however, the signaling pathway leading to p53 activation and renal apoptosis is unknown. Here we demonstrate an early DNA damage response during cisplatin treatment of renal cells and tissues.

WebDuring cisplatin treatment, p53 was activated. The inhibition of p53 by pifithrin-α attenuated the cisplatin-induced kidney injury and up-regulated miR-142-5p expression. We also identified the Sirtuin7 (SIRT7) as a target of miR-142-5p.

WebJul 1, 2024 · 1. Introduction. Cisplatin is widely and commonly used as a chemotherapeutic agent for the treatment of solid tumors, but the frequent occurrence of renal injury is the major limitation of cisplatin-based chemotherapy [1, 2].Renal proximal tubular damage due to activation of cell death and inflammatory pathways pathophysiologically characterizes … smalltown boy 12Webp53 mediates cisplatin-induced apoptosis in renal proximal tubular cells, and p53 can activate caspase-3 . Related to this, Li et al. described that HRPTEp cells treated with DDP for 48 h showed that DDP led to significantly upregulated miR-449a. In the same way, the overexpression of miR-449a led to an increased apoptotic rate of HRPTEpCs ... hild warrior nunWebJul 19, 2024 · Background Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths primarily due to chemoresistance. Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; > 30%) are major contributors to cisplatin (CDDP) resistance. Substantial evidence suggests the elevated levels of reactive oxygen species … smalltown 6 hild1957WebThe inhibition of p53 by pifithrin-α attenuated the cisplatin-induced kidney injury and up-regulated miR-142-5p expression. We also identified the Sirtuin7 (SIRT7) as a target of miR-142-5p. smalltown boy bronski beat lyricsWebThe average ID (50) (drug dose required to inhibit 50% of cell growth) for cell lines with mutant p53 was 6.8 microM, whereas the average ID (50) for cell lines with wild-type p53 … smalltown beatWebFeb 28, 2024 · Our data revealed that p53 inhibition could attenuate cisplatin-induced acute kidney injury by up-regulating miR-142-5p to repress SIRT7/NF-κB. These findings may provide a novel therapeutic target of cisplatin-induced acute kidney injury. Keywords: Acute kidney injury, cisplatin, miR-142-5p, p53 Introduction hild\\u0027s marine