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Cisplatin p53

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 ... 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

Medicina Free Full-Text Evaluating the Magnolol Anticancer ...

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 … 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 … tailwindcss template blog https://bassfamilyfarms.com

Medicina Free Full-Text Evaluating the Magnolol …

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. WebMay 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. 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 … tailwind css text

Molecules Free Full-Text Enhancement of Cisplatin …

Category:p53 inhibition attenuates cisplatin-induced acute kidney injury …

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Cisplatin p53

Frontiers Scutellarin Increases Cisplatin-Induced Apoptosis …

WebFeb 13, 2024 · Cisplatin, as the first-line anti-tumor agent, is widely used for treatment of a variety of malignancies including non-small cell lung cancer (NSCLC). However, the acquired resistance has been a major obstacle for the clinical application. Scutellarin is a active flavone extracted from Erigeron breviscapus Hand-Mazz that has been shown to … 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...

Cisplatin p53

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WebMay 7, 2024 · Consistently, genetic depletion or pharmacological inhibition of USP10 dramatically reduces the growth of lung cancer xenografts lacking wild-type p53 and sensitizes them to cisplatin.... 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 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 ...

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 … 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 ].

WebHistopathological examination of cardiac muscles of all studied groups and immunoassay of P53 and caspase 3 in cardiac tissue were examined to assess apoptosis. Cisplatin has … 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 …

WebMay 26, 1998 · The p53-mutant mouse teratocarcinoma cells did not undergo cisplatin-induced apoptosis, although clonogenic assays revealed an overall sensitivity similar to …

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... tailwind css text boldWebHistopathological examination of cardiac muscles of all studied groups and immunoassay of P53 and caspase 3 in cardiac tissue were examined to assess apoptosis. Cisplatin has disturbed mitochondrial function and dynamics, dysregulate redox status and induced mitophagy and apoptosis, in the other hand semaglutide treatment has normalized ... twin falls home and garden show 2023WebThe 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 … tailwind css text-indentWebJul 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 ... tailwind css text spacingWebNational Center for Biotechnology Information tailwind css text centerWebMay 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. twin falls hiking trailWebIC50 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. tailwind css text ellipsis