2024 Cisplatin p53

Cisplatin p53

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August undefined, 2024

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. 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 ...

The cardioprotective effect of human glucagon-like …

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 … metabox531

p53-dependent and -independent responses to cisplatin in mouse …

WebNational Center for Biotechnology Information 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.... metabox543

Fenofibrate reduces cisplatin-induced apoptosis by inhibiting the p53 …

Cisplatin-induced apoptosis in BUMPT cells. (A) BUMPT cells were ...

WebOct 28, 2024 · The mutational status of p53 seems to be related to the preferential response of tumor cells to Wee1 inhibitors 21 – 23. Studies have shown that AZD1775 radiosensitized p53-defective human cells derived from lung, breast, and prostate cancers by abrogating the radiation-induced G2 block, while this was not observed in p53 wild-type cells 24 ... 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 metabox541WebOct 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 ... metabox544

"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. " - Cisplatin p53

Cisplatin p53

p53-dependent and -independent responses to cisplatin in mouse …

WebFeb 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... 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 …

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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 ]. 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...

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 … 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 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... 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.

WebApr 11, 2024 · 2024年查处的不端行为案件处理结果通报（第一批次）. 近期，经国家自然科学基金委员会监督委员会调查审议、国家自然科学基金委员会委务会议审定，国家自然科学基金委员会对相关科研不端案件涉事主体进行了处理。. 现将给予通报批评的有关案情及处理 ...

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. metabox534WebFeb 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. metabox538WebJul 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 ... how tall was eve islamWebCisplatin 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 … how tall was eren\u0027s founding titanWebWe 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 the amyloid-state of mutant p53 may be an attractive therapeutic approach for HCC, and highlight PRIMA-1 as a new candidate for combination therapy with cisplatin. how tall was eric flemingWebω-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. how tall was fanny brawneWebThe 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 … how tall was erin moran