The tumor suppressor p53 is a negative regulator of the carcinoma-associated transcription factor FOXQ1
These videos have been matched automatically. Contact us if they are not relevant.
These videos have been matched automatically. Contact us if they are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.The tumor suppressor p53 negatively regulates FOXQ1 expression, a factor driving cancer metastasis. Loss of p53 function in cancer leads to increased FOXQ1, promoting tumor progression.
Area Of Science
- Molecular biology
- Cancer research
- Genetics
Background
- Forkhead box Q1 (FOXQ1) is upregulated in carcinomas, promoting epithelial-to-mesenchymal transition and metastasis.
- Mechanisms of FOXQ1 deregulation in cancer are not fully understood.
Purpose Of The Study
- To identify transcriptional regulators of FOXQ1.
- To elucidate the role of p53 in FOXQ1 expression and its implications in cancer.
Main Methods
- CRISPR-Cas9-based genomic locus proteomics.
- Promoter reporter assays.
- Chromatin immunoprecipitation followed by quantitative PCR (ChIP-qPCR).
- Gain and loss-of-function assays.
- Pharmacological activation of p53.
Main Results
- The tumor suppressor p53 was identified as a negative regulator of FOXQ1 expression.
- p53 binds near the FOXQ1 promoter and suppresses its transcription.
- Pharmacological p53 activation reduced FOXQ1 levels in wildtype p53 cancer cells.
- p53 mutations correlate with increased FOXQ1 expression in human cancers.
Conclusions
- Loss of p53 function derepresses FOXQ1, contributing to tumor progression.
- p53 acts as a critical suppressor of FOXQ1, impacting cancer metastasis.
These videos have been matched automatically. Contact us if they are not relevant.
These videos have been matched automatically. Contact us if they are not relevant.
Related Concept Videos
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Three of the best-understood negative regulators are p53, p21, and retinoblastoma protein (Rb). The regulatory roles of each of these proteins were discovered after faulty copies were found in cells with uncontrolled replication (i.e.,...
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...