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Updated: Dec 20, 2025

Analysis of Cell Cycle Position in Mammalian Cells
Published on: January 21, 2012
Multiple Functions of Fubp1 in Cell Cycle Progression and Cell Survival
Mingyu Kang1, Hyeon Ji Kim1, Tae-Jun Kim1
1Department of Pharmacology, School of Dentistry, Kyungpook National University, 700-412 Daegu, Korea.
Abstract:
The discovery of novel and critical genes implicated in malignant development is a topic of high interest in cancer research. Intriguingly, a group of genes named "double-agent" genes were reported to have both oncogenic and tumor-suppressive functions. To date, less than 100 "double-agent" genes have been documented. Fubp1 is a master transcriptional regulator of a subset of genes by interacting with a far upstream element (FUSE). Mounting evidence has collectively demonstrated both the oncogenic and tumor suppressive roles of Fubp1 and the debate regarding its roles in tumorigenesis has been around for several years. Therefore, the detailed molecular mechanisms of Fubp1 need to be determined in each context. In the present study, we showed that the Fubp1 protein level was enriched in the S phase and we identified that Fubp1 deficiency altered cell cycle progression, especially in the S phase, by downregulating the mRNA expression levels of Ccna genes encoding cyclin A. Although this Fubp1-cyclin A axis appears to exist in several types of tumors, Fubp1 showed heterogeneous expression patterns among various cancer tissues, suggesting it exhibits multiple and complicated functions in cancer development. In addition, we showed that Fubp1 deficiency confers survival advantages to cells against metabolic stress and anti-cancer drugs, suggesting that Fubp1 may play both positive and negative roles in malignant development.
Insights
The study reveals that Fubp1 protein levels are high during S phase, impacting cell cycle progression. Fubp1 deficiency offers cancer cells survival advantages against stress and drugs, highlighting its dual role in cancer.
Area of Science:
- Molecular biology
- Cancer research
- Cell cycle regulation
Background:
- Double-agent genes possess both oncogenic and tumor-suppressive functions, with fewer than 100 documented.
- Fubp1 acts as a master transcriptional regulator by interacting with the FUSE element.
- Fubp1's dual roles in tumorigenesis are debated, necessitating detailed mechanistic studies.
Purpose of the Study:
- To investigate the molecular mechanisms of Fubp1 in cancer development.
- To determine the role of Fubp1 in cell cycle progression and its association with cyclin A.
- To explore Fubp1's impact on cancer cell survival under stress and drug treatment.
Main Methods:
- Analysis of Fubp1 protein levels during the cell cycle.
- Assessment of Fubp1's effect on cell cycle progression, particularly S phase.
- Quantification of Ccna gene (cyclin A) mRNA expression in Fubp1-deficient cells.
- Evaluation of Fubp1's influence on cancer cell survival against metabolic stress and anti-cancer drugs.
Main Results:
- Fubp1 protein levels are enriched in the S phase of the cell cycle.
- Fubp1 deficiency alters cell cycle progression, specifically downregulating cyclin A (Ccna) mRNA expression.
- Fubp1 exhibits heterogeneous expression across various cancer tissues, indicating complex functions.
- Fubp1 deficiency enhances cancer cell survival against metabolic stress and anti-cancer drugs.
Conclusions:
- Fubp1 plays a critical role in regulating cell cycle progression, particularly during S phase, via the cyclin A pathway.
- Fubp1's expression pattern and functions are context-dependent and heterogeneous across different cancers.
- Fubp1 deficiency confers a survival advantage to cancer cells, suggesting a complex, potentially dual role in malignant development.
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