Cisplatin p53

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. 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 …

p53 sensitizes chemoresistant non-small cell lung cancer via …

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 ... WebIC50 values indicated less toxicity of the Schiff base complex on GMSCs compared to cisplatin. Schiff base complex treatment resulted in up-regulation of p53 and Bax genes expression and down-regulation of Bcl2 gene expression in SCCs paralleled with increased protein expression of caspase-3 and Bax and down-regulation of Bcl-2 protein. how many rainy days in seattle https://dalpinesolutions.com

Frontiers PRIMA-1 inhibits Y220C p53 amyloid …

WebWhen p53 was inhibited by 20 μM pifithrin-α (PFT-α) (Sigma-Aldrich) in cisplatin-treated cells and the expression levels of glycolysis-related genes were determined by qRT-PCR ( Fig 5 B), it... WebMay 26, 1998 · The p53-mutant mouse teratocarcinoma cells did not undergo cisplatin-induced apoptosis, although clonogenic assays revealed an overall sensitivity similar to … 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 ]. how many raisins can a diabetic eat

Frontiers PRIMA-1 inhibits Y220C p53 amyloid …

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Cisplatin p53

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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. 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

Cisplatin p53

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WebCisplatin inhibited glycolysis via p53 activation. (A) Western blot analysis indicated increased levels of p53 and phospho-p53 after 6 and 24 h of cisplatin treatment. The … WebSpecifically, E1A/Ras- transformed S47 cells show increased sensitivity to cisplatin and paclitaxel, and comparable transactivation of GLS2 and SCO2, compared to cells with WT p53.

WebFeb 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 WebThe 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.

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 … WebJan 30, 2024 · (D) Mechanism that CKI sensitizes p53-mutant CRC cells to cisplatin. The R273H/P309S mutation of p53 rendered CRC cells insensitive to Cis and 5FU treatments. The in vitro anti-CRC profiles of CKI + Cis combination were distinct from that of CKI+5FU. CKI decreased drug sensitivity to 5FU in both p53 wild and R273H/P309S mutation CRC …

WebFeb 28, 2024 · The p53 signaling pathway is involved in cisplatin-induced acute kidney injury (AKI). Western blot analysis showed that p53 was activated in the kidney ( Figures …

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 … how many raisins in a miniature boxWebSep 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, … how deep is earth\u0027s crust milesWebMay 26, 2006 · In the p53- and MMR-proficient cells, cisplatin induced a 17-fold increase in homologous recombination even when the recombining sequences that did not contain cisplatin adducts; the magnitude of induction was even greater in cells that had lost either one or both functions. how many raisins dogs toxicWebNational Center for Biotechnology Information how deep is footingWebJan 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 … how deep is flathead lake mtWebMay 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. how deep is fowey harbourWebp53 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 ... how deep is gas line to house