scispace - formally typeset
Search or ask a question

What are the functions wildtype p53 has in cancer? 


Best insight from top research papers

Wild-type p53 (wtp53) in cancer plays crucial roles in regulating various cellular processes. It functions in DNA repair, cell cycle arrest, apoptosis induction, metabolic changes, and aging, acting as a tumor suppressor . Mutations in the TP53 gene can lead to loss of these functions, contributing to oncogenic processes and cancer development . Additionally, wtp53 influences redox homeostasis, metabolic stability, and intracellular ferroptosis, impacting cancer cell growth . The abnormal signaling of the p53 pathway in cancer cells, often due to factors like high MDM2 expression, underscores the significance of wtp53 as a target for cancer treatment strategies . Targeting wild-type and mutant p53 for cancer therapy has shown promise through various approaches, highlighting the importance of understanding p53's functions in cancer progression and treatment .

Answers from top 5 papers

More filters
Papers (5)Insight
Wild-type p53 in cancer functions include growth suppression, cell death, DNA repair, and metabolism regulation, making it a key tumor suppressor.
Wildtype p53 in cancer functions as a tumor suppressor by promoting cell survival through DNA repair or inducing apoptosis if DNA damage is irreparable, preventing cancer progression.
Journal ArticleDOI
01 Aug 2022
Wildtype p53 functions in cancer by regulating cell cycle, inducing senescence, apoptosis, and metabolic reprogramming, inhibiting tumor growth, and maintaining redox homeostasis, but mutant p53 may impair these functions.
Wildtype p53 in cancer maintains genetic stability, regulates cell cycle, programmed cell death, DNA repair, aging, and angiogenesis, acting as a crucial tumor suppressor protein.
Wild-type p53 in cancer regulates DNA repair, cell cycle, apoptosis, metabolism, and aging. It serves as a biomarker for tumor progression and a target for cancer therapy.

Related Questions

What is the role of p53 signaling pathway in immune cells?5 answersThe p53 signaling pathway plays a crucial role in immune cells by impacting various aspects of immune responses. Studies have shown that p53 is involved in detecting danger signals, inflammasome formation, antigen presentation, activation of natural killer cells, interferon production, inhibition of virus replication, and modulation of immune-related signaling pathways. Additionally, p53 can influence antitumor T cell immunity by reprogramming the tumor microenvironment through tumor-associated macrophages, leading to enhanced responses to immune checkpoint blockade. Furthermore, p53's regulatory functions extend to inflammatory responses, cytokine induction, Toll-like receptor modulation, and immune cell differentiation and maturation, highlighting its broad impact on immune system regulation. Overall, p53 signaling pathway emerges as a multifaceted regulator of immune responses with implications for cancer immunology, virology, and autoimmune diseases like rheumatoid arthritis.
How does p53 affect cancer?5 answersp53 is a critical tumor suppressor protein that plays a role in maintaining genetic stability and controlling various cellular processes. Mutations in p53 can lead to genetic instability and contribute to carcinogenesis. In breast cancer, p53 mutations are associated with poorer prognosis, particularly in hormone receptor-negative subtypes. Mutant p53 can have gain-of-function oncogenic activities that promote tumorigenesis and progression. The stabilization of mutant p53 is regulated by molecular chaperones and the ubiquitin-proteasome system, which contribute to its accumulation in tumor cells. The formation of p53 amyloids is also observed in cancer tissues and is correlated with cancer grades and loss of p53 function. Targeting both wild-type and mutant p53 has clinical relevance in breast cancer treatment. Understanding the mechanisms of p53 function and regulation is crucial for developing p53-based therapies for cancer treatment.
What is the role of TP53?5 answersTP53 plays a crucial role in cancer formation and is considered the most important tumor suppressor gene. It acts as a transcription factor involved in DNA repair, cell-cycle control, and apoptosis. TP53 is commonly mutated in various cancers, including prostate adenocarcinoma (PRAD), brain lower-grade glioma (LGG), uterine carcinosarcoma (UCS), and uterine corpus endometrial carcinoma (UCEC). The expression level of TP53 is significantly different in tumor tissues compared to normal tissues, with high expression in most malignant tumors. TP53 mutations can affect the immune response in different cancers, and its expression is associated with immune cell infiltration and immune scores. In ovarian cancer, TP53 mutation status influences the expression of repetitive elements (REs) following epigenetic treatment, and TP53 mutant cell lines have higher baseline expression of REs compared to wild-type cell lines. TP53 mutation serves as a biomarker, prognostic factor, and therapeutic target in colorectal cancer.
What is the role of p53 in hereditary breast cancer?5 answersThe p53 protein plays a crucial role in hereditary breast cancer. TP53 mutations are prevalent in nearly all tumors, including breast cancer, and are the primary genetic lesions found in Li-Fraumeni Syndrome (LFS). Somatic mutations in TP53 are also common in sporadic breast cancers, particularly in the triple-negative subtype. The breast epithelium appears to be uniquely sensitive to alterations in p53 function, as breast cancer is the most common tumor among women with inherited TP53 mutations. Missense mutations in TP53, especially those affecting codons R175, G245, R248, and R273, are associated with dominant-negative activities and impaired function of the p53 pathway. The mutational spectrum of TP53 in breast cancer includes missense mutations, nonsense mutations, frameshift mutations, splice mutations, and deletions, all of which lead to loss of function. Therefore, p53 mutations contribute to the development and progression of hereditary breast cancer.
How does p53 function in cancer?3 answersp53 is a tumor suppressor gene that plays a crucial role in regulating cancer cell behavior. Mutations in p53 are found in more than 50% of human cancers, leading to loss of its tumor suppressor function. p53 responds to various stresses such as DNA damage, oncogene activation, and oxidative stress by inducing cellular responses like cell cycle arrest, apoptosis, and cellular senescence. It also regulates energy metabolism, including glycolysis, mitochondrial respiration, amino acid metabolism, fatty acid metabolism, and autophagy. Additionally, p53 mutations can result in the gain of novel oncogenic functions, contributing to tumor development and modifying cellular metabolism. The multifunctionality of p53, particularly in intracellular metabolisms, makes it a key molecule in cancer and metabolic disorders.
What are the different isoforms of p53 and what are their roles in the cell?5 answersThe p53 protein has multiple isoforms that play different roles in the cell. These isoforms arise from alternative splicing, alternative initiation of translation, and alternative promoter usage. The isoform p53/47 lacks the first 40 codons and is linked to endoplasmic reticulum stress and a specific G2 arrest. Another isoform, Δ133p53, lacks the first 133 amino acids and is involved in controlling cellular senescence. The isoform p53β carries an alternative C-terminus and is also implicated in controlling cellular senescence. Additionally, there are isoforms Δ40p53 and Δ133p53 that interact with p53 and have antagonist effects. Some p53 isoforms act in a dominant-negative manner, interfering with the function of full-length p53. The precise functions of p53 isoforms are still being discovered, but they are known to be involved in various cellular processes such as DNA repair, cell cycle arrest, apoptosis, and gene expression modulation.

See what other people are reading

How was digoxin in the treatment of breast cancer?
5 answers
Digoxin has shown promising potential in the treatment of breast cancer through various mechanisms. Studies have demonstrated that digoxin induces ERα degradation, inhibits 17β-estradiol signaling, triggers apoptosis, and blocks cell cycle progression in breast cancer cells, both primary and metastatic. Additionally, digoxin has been found to inhibit the growth of breast cancer cells by inducing mitochondria-dependent apoptosis, reducing Bcl-2 expression, and increasing Bax levels. Furthermore, digoxin and its synthetic analog MonoD have shown cytotoxic effects on triple-negative breast cancer cells by increasing cell cycle arrest, reducing cell viability, inhibiting migration, inducing apoptosis, and modulating the nuclear factor kappa B pathway. These findings collectively suggest that digoxin holds promise as a potential therapeutic agent for breast cancer treatment.
What is the semiconservative replication in DNA?
4 answers
Semiconservative DNA replication is a fundamental process where each newly synthesized DNA strand contains one original parental strand and one newly synthesized complementary strand. This mechanism allows for accurate transmission of genetic information. The presence of short tandem repeats (STRs) and simple sequence repeats (SSRs) in genomes across various species suggests a continuous production of repeats during replication, contributing to a semi-conservative replicating process. The folded replication slippage model, which considers nucleotide geometry and hydrogen bond stability, provides a more detailed explanation for the expansion and contraction of these repeats, with a tendency for expansion observed in microsatellites. Asymmetries inherent in DNA replication also play crucial roles in adaptation, evolution, and cell fate decisions, highlighting the complexity and significance of this essential biological process.
What are the implications of BRCA1 mutation on the efficacy of personalized therapeutic interventions for breast cancer?
5 answers
BRCA1 mutations play a significant role in the efficacy of personalized therapeutic interventions for breast cancer. Mutations in BRCA1 lead to DNA repair defects, making tumors more vulnerable to therapies like Poly (ADP-ribose) polymerase inhibitors (PARPi). These mutations result in homologous recombination repair deficiencies, affecting responses to platinum salt therapies and PARP inhibitors. However, the efficacy of these treatments can be impacted by the development of resistance due to interconnected DNA repair pathways compensating for each other. Additionally, BRCA1 promoter methylation can lead to poor outcomes and adaptive chemoresistance, altering therapeutic responses in TNBC and ovarian cancers. Understanding the implications of BRCA1 mutations is crucial for tailoring effective treatment strategies in breast cancer patients.
What are the cancers associated with tp53 (R248Q) mutation?
5 answers
The TP53 mutation R248Q is associated with various cancers, including breast cancer, head and neck squamous cell carcinomas (HNSCC), and multiple malignant tumors. In breast cancer, TP53 mutations are linked to aggressive behavior and resistance to treatments like chemotherapy and radiotherapy. In HNSCC, TP53 mutations are identified as the most frequent somatic genomic alterations, contributing to tumor aggressiveness and reduced survival post-surgery. Additionally, a comprehensive analysis across different cancers revealed that the TP53 mutation R248Q is reported in 51 types of tissues, indicating its widespread presence and potential impact on tumorigenesis. These findings underscore the significance of TP53 mutations, such as R248Q, in driving oncogenesis and influencing treatment outcomes in various cancer types.
Candida genomic and functional
5 answers
Candida species, including Candida albicans and Candida glabrata, exhibit remarkable genomic diversity and functional adaptations that contribute to their pathogenicity. Studies have highlighted the importance of gene editing techniques like CRISPR-Cas9 and high-efficient transposons in advancing the understanding of Candida molecular biology. Additionally, the BioFung database and carbohydrate-active enzyme analysis have revealed core metabolic pathways and biomarkers in Candida species, emphasizing their metabolic plasticity and adaptation to different environments. Furthermore, research on Candida glabrata has shown its evolution of stress resistance mechanisms, enabling survival against host immune defenses and antifungal drugs. The genomic arrangement in Candida albicans involves clustering of co-regulated genes, facilitating coordinated transcription and functional gene expression. These findings collectively underscore the intricate genomic and functional intricacies of Candida species in causing infections and adapting to diverse environments.
Is tween 20 milder than triton x-100 towards bacteria?
5 answers
Tween 20 and Triton X-100 are both surfactants with varying effects on bacteria. Tween 20, similar to Tween 80, is a non-ionic surfactant that can enhance antibacterial properties when combined with chitosan membranes. On the other hand, Triton X-100, specifically Triton A20, has been shown to have different effects on bacterial cultures, such as promoting dispersed growth of tubercle bacilli and influencing bacterial morphology. Additionally, Tween 80 has been tested for its impact on DNA repair in Escherichia coli, showing no significant changes in cell growth or DNA repair processes. Overall, based on the available data, Tween 20 appears to have milder effects on bacteria compared to Triton X-100, particularly Triton A20, which has shown specific interactions with bacterial growth and morphology.
Are mutations always negative?
5 answers
Mutations are not always negative; they can have various impacts depending on the context. While some mutations can be harmful, leading to decreased cell survival or driving tumor growth, others can actually provide evolutionary advantages, such as in the case of negative epistasis influencing the evolution of sex and recombination. Additionally, mutations changing a protein's surface chemistry can impact its self-assembly and localization in cells, highlighting the complex nature of genotype-phenotype relationships. It is essential to understand that mutations can have diverse effects, ranging from detrimental to beneficial, depending on the specific genetic context and the biological system under consideration.
What are the potential mechanisms underlying the association between ICIP and TMB, and how might these influence treatment decisions?
5 answers
The association between immune checkpoint inhibitor therapy (ICI) and tumor mutational burden (TMB) involves several key mechanisms. High TMB has been linked to improved survival with ICI treatment, but not all high-TMB patients respond well. Specific gene alterations impact outcomes differently in TMB-high and TMB-low patients, influencing response to ICI. For instance, mutations in genes like STK11 and E2F3 are associated with worse outcomes in TMB-high tumors, while mutations in genes like NTRK and PTPRD are linked to better outcomes. Additionally, the immune-excluded phenotype, characterized by high stromal TIL and low intratumoral TIL density, is correlated with high TGFBs and poor response to immunotherapy. These insights can guide treatment decisions by helping identify patients likely to benefit from ICI based on their TMB status and specific gene alterations.
What is the role of mitotic index in mutagenesis assay?
4 answers
The mitotic index (MI) plays a crucial role in mutagenesis assays by serving as a standard cytotoxic parameter for evaluating test concentrations for chromosome aberrations. MI estimation, expressed as a percentage of mitotic cells, is essential for determining the impact of candidate agents on cell proliferation and genotoxic effects. Utilizing automated tools like CellProfiler for MI assessment enhances accuracy and efficiency in detecting mitotic figures, reducing variability and saving time compared to manual methods. Automation of MI assessment using flow cytometry with markers like phosphorylated-histone H3 enables precise measurement of MI frequencies in chemically-treated cell cultures, providing a reliable alternative to traditional microscopic analysis. In the context of mutagenesis assays, the MI serves as a valuable indicator of cellular response to genotoxic agents, aiding in the evaluation of potential mutagenic effects.
How to conduct mixed biological replicates in plant biology for qPCR?
5 answers
To conduct mixed biological replicates in plant biology for qPCR, it is crucial to optimize the workflow to minimize technical variability and ensure reliable results. One approach is to increase the number of replicates based on the tissue type used. For instance, more RT replicates are recommended for leaf tissue, while more sampling replicates are advised for stems or fruits to enhance result accuracy. Additionally, employing a sensitive and high-throughput qPCR-based method can accurately detect gene-edited mutants in various plant species, allowing for the simultaneous analysis of multiple samples without post-PCR handling. Ensuring RNA quality, integrity, and compliance with MIQE guidelines are essential steps in optimizing the protocol for gene expression analysis in plant tissues, which has been successfully applied across different plant species.
Which markes can used for lung damage by particles in urine ?
10 answers
Markers for lung damage due to particle exposure can be identified and monitored through various substances found in urine, offering a non-invasive method for detecting lung injury. Hydroxylysine, a marker of connective tissue metabolism, has been identified as a potential early marker of lung injury related to exposure to atmospheric pollutants like nitrogen dioxide, indicating its utility in assessing damage from particle exposure. Additionally, the study of lung epithelium-specific DNA methylation patterns has led to the development of PCR sequencing assays that can detect lung-derived cell-free DNA (cfDNA) in the plasma, which, while not directly applicable to urine, suggests that similar methodologies could be adapted for urine-based detection of lung injury. The search for novel markers of lung injury has also highlighted the potential of urine as a non-invasive matrix for diagnostic biomarker development, with a study identifying a three-biomarker panel consisting of IGFBP-1, sIL-1Ra, and CEACAM-1 that discriminated non-small cell lung cancer (NSCLC) from healthy controls. This indicates the broader potential of urine biomarkers in lung damage detection. Furthermore, the use of urine for monitoring children's respiratory health has been explored, with Club cell protein (CC16), osteopontin (OPN), and nuclear factor-kappa B (NF-κB) identified as biomarkers of lung diseases and adverse effects towards the airway epithelium integrity. This approach necessitates proper adjustment for physiological confounders influencing urinary excretion, suggesting a complex but feasible method for detecting lung damage through urine. Lastly, the exploration of volatile biomarkers in the headspace air of lung alveolar cells exposed to quartz particles has identified metabolites related to oxidative and lipid peroxidation of the cell membrane, indicating potential volatile biomarkers for particulate-induced lung injury that could be adapted for urine analysis. In summary, while direct urine markers for lung damage by particles include hydroxylysine and potentially a panel of IGFBP-1, sIL-1Ra, and CEACAM-1, ongoing research into DNA methylation patterns, volatile biomarkers, and proteins related to lung epithelium integrity suggests a growing field of urine-based diagnostics for lung injury detection.