ArticleClinics (Sao Paulo, Brazil)2013
Prima-1 induces apoptosis in bladder cancer cell lines by activating p53.
Article in Clinics (Sao Paulo, Brazil), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- The Effect of Arbutin on The Expression of Tumor SuppressorCell journal · 2021Article
- p53 reactivation with induction of massive apoptosis-1 (PRIMA-1) inhibits amyloid aggregation of mutant p53 in cancer cells.The Journal of biological chemistry · 2019Article
- PRIMA-1 and PRIMA-1Cancers · 2017Review
- Mutant p53 Protein and the Hippo Transducers YAP and TAZ: A Critical Oncogenic Node in Human Cancers.International journal of molecular sciences · 2017Review
- Molecular targets in urothelial cancer: detection, treatment, and animal models of bladder cancer.Drug design, development and therapy · 2016Review
- Oncogenic Intra-p53 Family Member Interactions in Human Cancers.Frontiers in oncology · 2016Review
- MicroRNA-155 promotes bladder cancer growth by repressing the tumor suppressor DMTF1.Oncotarget · 2015Article
- p53 Family and Cellular Stress Responses in Cancer.Frontiers in oncology · 2014Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesBladder cancer represents 3% of all carcinomas in the Brazilian population and ranks second in incidence among urological tumors, after prostate cancer. The loss of p53 function is the main genetic alteration related to the development of high-grade muscle-invasive disease. Prima-1 is a small molecule that restores tumor suppressor function to mutant p53 and induces cancer cell death in various cancer types. Our aim was to investigate the ability of Prima-1 to induce apoptosis after DNA damage in bladder cancer cell lines.
methodThe therapeutic effect of Prima-1 was studied in two bladder cancer cell lines: T24, which is characterized by a p53 mutation, and RT4, which is the wild-type for the p53 gene. Morphological features of apoptosis induced by p53, including mitochondrial membrane potential changes and the expression of thirteen genes involved in apoptosis, were assessed by microscopic observation and quantitative real-time PCR (qRT-PCR).
resultsPrima-1 was able to reactivate p53 function in the T24 (p53 mt) bladder cancer cell line and promote apoptosis via the induction of Bax and Puma expression, activation of the caspase cascade and disruption of the mitochondrial membrane in a BAK-independent manner.
conclusionPrima-1 is able to restore the transcriptional activity of p53. Experimental studies in vivo may be conducted to test this molecule as a new therapeutic agent for urothelial carcinomas of the bladder, which characteristically harbor p53 mutations.
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