Related Experiment Video
Updated: Oct 25, 2025
08:54
An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
Published on: July 20, 2014
14.2K
A p53/CPEB2 negative feedback loop regulates renal cancer cell proliferation and migration
Jiehui Di1, Guang Zhao2, Hui Wang2
1School of Life Science and Technology, Harbin Institute of Technology, Harbin, Heilongjiang 150001, China; Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China; Center of Clinical Oncology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, China; Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu 221002, China.
Journal of Genetics and Genomics = Yi Chuan Xue Bao
|August 7, 2021
Summary
The tumor suppressor p53 gene is targeted by RNA-binding protein CPEB2, which then reduces p53 levels. This feedback loop promotes renal cancer progression by inactivating p53.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- The tumor suppressor p53 is crucial for maintaining genome stability by regulating gene expression.
- Cancer cells often develop mechanisms to evade p53-mediated cell cycle checkpoints.
- Understanding novel regulatory pathways involving p53 is essential for cancer therapy.
Purpose of the Study:
- To identify novel p53 target genes involved in regulating p53 levels.
- To investigate the role of cytoplasmic polyadenylation element-binding protein 2 (CPEB2) in p53 regulation.
- To determine the impact of the p53-CPEB2 interaction on renal cancer progression.
Main Methods:
- Identified CPEB2 as a p53 target gene using molecular biology techniques.
- Investigated CPEB2's effect on p53 mRNA stability and translation.
- Analyzed CPEB2 binding to the p53 3'-untranslated region using RNA-binding assays.
- Examined CPEB2 expression in renal cancer tissues and assessed its functional role in cell proliferation and migration.
Main Results:
- CPEB2 directly binds to cytoplasmic polyadenylation elements in the p53 3'-untranslated region via its RNA recognition motif and zinc finger domains.
- CPEB2 decreases p53 mRNA stability and translation, creating a negative feedback loop.
- CPEB2 is upregulated in renal cancer and promotes tumor cell proliferation and migration.
- The oncogenic effects of CPEB2 are partially mediated by the inactivation of p53.
Conclusions:
- A novel feedback loop between p53 and CPEB2 has been identified.
- CPEB2 promotes renal cancer progression by negatively regulating p53.
- CPEB2 represents a potential therapeutic target for human renal cancer.
Related Concept Videos
02:23Abnormal Proliferation
4.8K
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...
4.8K
01:23Negative Regulator Molecules
36.7K
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.
36.7K
03:03mTOR Signaling and Cancer Progression
4.0K
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...
The mTOR pathway or the...
4.0K
01:19Interactions Between Signaling Pathways
6.7K
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...
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...
6.7K
02:34Inhibition of Cdk Activity
5.1K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.1K
02:39Positive Regulator Molecules
5.9K
Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
5.9K