Our present study provides compelling evidence that pharmacological activation of the p53 by blocking the MDM2-p53 interaction is a promising cancer therapeutic strategy and using RITA in combination with Cisplatin not only decrease the toxic effect of Cisplatin by decreasing its dose but also increasing the apoptotic effect, warrants clinical evaluation on both colon and prostate cancer.
The goal of this study was to evaluate the effects of 8-wk aerobic exercise training and administration of green tea extract on the level of nuclear factor kappa B (NF-kB), cyclooxygenase-2 (COX-2) and p53 tumor suppressor protein (p53) in prostate of rats which were stimulated by N-methyl-N-nitrosourea to induce the prostate cancer.
Prostate cancer is a common health problem among men worldwide and most of these prostate cancer cases are related to a dysfunctional mutant Tumor Protein p53 (TP53) gene.
At the same time, a series of transcription factors (relating to RELA, SOX10, TP53, and TWIST2, etc.) were obtained and may play a key regulatory role in prostate cancer PC-3 cell-related modules.
The data presented here suggest a therapeutic potential of targeting mutant p53 protein in advanced PCa setting, which has a clinical impact for aggressive PCa with transforming how such tumors are managed.
Recent genome analysis of human prostate cancers demonstrated that both AR gene amplification and TP53 mutation are among the most frequently observed alterations in advanced prostate cancer.
We demonstrated that PEITC inhibits the growth of prostate cancer cells with different "hotspot" p53 mutations (structural and contact), however, preferentially towards structural mutants.
Our data, therefore, suggest that enzalutamide's high efficacy is at least partially independent of AR and p53 protein expression, which are frequently lost in advanced PC.
Overall, no association was observed between TP53 gene codon72 polymorphism and prostate cancer risk (Arg vs Pro: odds ratio [OR] = 1.12, 95% confidence interval [CI] = 0.98-1.30; ArgArg vs ProPro: OR = 1.26, 95% CI = 0.90-1.75; ProPro vs ArgArg+ ArgPro: OR = 1.17, 95% CI = 0.86-1.57; ArgPro+ ProPro vs ArgArg: OR = 1.21, 95% CI = 0.97-1.51).
The goal of this study was to evaluate the effects of eight-week aerobic exercise training and administration of green tea extract on the level of nuclear factor kappa B (NF-kB), cyclooxygenase-2 (COX-2) and p53 tumor suppressor protein (p53) in prostate of rats which were stimulated by N-Methyl-N-nitrosourea (NMU) to induce the prostate cancer.
Our results indicate that targeting ACO2 through zinc and p53 can change prostate cancer metabolism, and thus provides a potential new therapeutic strategy for prostate cancer.
Further top five genes viz Rhoa, PI3KCA, CDC42, MAPK3, TP53 were used for Enrichment analysis which revealed their association with vital cellular and functional pathways in prostate cancer indicating their potential as candidate biomarkers in prostate cancer.
While PTEN inactivation leads to PC, it is not sufficient for metastasis, the loss of PTEN concurrently with the inactivation of both TP53 and RB1 empower lineage plasticity in PC cells, which substantially promotes PC metastasis and the conversion to PC adenocarcinoma to neuroendocrine PC (NEPC), demonstrating the essential function of TP53 and RB1 in the suppression of PCSCs.
TP53 mutation is associated with higher tumor-infiltrating T-cell density, which may be relevant in future clinical trials of immunotherapy in prostate cancer.
Prostate cancer cell lines LNCaP and PC3 were treated with X-rays and AICAR then assessed for clonogenic survival, spheroid growth delay, cell cycle progression, and AMPK and p53 activity.
In this study, we found that hexokinase 2 (HK2), which has dual metabolic and apoptotic functions, is downstream of zinc and p53 in both prostate cancer patient tissue and prostate cancer cell lines.
Thus, we concluded that p53 is a sensor for enhanced apoptosis in response to DNA damage stress, not DNA replication stress, at least in prostate cancer.
Although Ad-p53 gene therapy has yielded some interesting results when applied to prostate cancer, it has not been widely explored, perhaps due to current limitations of the approach.