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CREB3L1/OASIS: cell cycle regulator and tumor suppressor
Atsushi Saito1, Issei Omura1, Kazunori Imaizumi1
1Department of Biochemistry, Institute of Biomedical & Health Sciences, Hiroshima University, Japan.
The FEBS Journal
|January 12, 2024
Summary
Old astrocyte specifically induced substance (OASIS), an ER-resident transcription factor, plays a novel role in cell cycle regulation. OASIS induces p21-mediated cell cycle arrest in response to DNA damage, distinct from p53 pathways.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Cell cycle checkpoints are crucial for DNA repair; their failure leads to diseases like cancer.
- Endoplasmic reticulum (ER) stress transducers, like CREB3L1 (OASIS), regulate cellular processes including differentiation and metabolism.
- OASIS, an ER-resident transcription factor, is activated via regulated intramembrane proteolysis.
Purpose of the Study:
- To summarize the previously unknown roles of OASIS in cell cycle regulation.
- To explore the commonalities and differences between OASIS and p53 in inducing cell cycle arrest.
- To discuss the implications of OASIS dysfunction in tumorigenesis and its potential as a therapeutic target.
Main Methods:
- Literature review focusing on ER stress, cell cycle checkpoints, and transcription factors.
- Analysis of OASIS activation pathways in response to DNA damage.
- Comparison of OASIS and p53-mediated cell cycle arrest mechanisms.
Main Results:
- OASIS is activated by DNA damage to induce p21-mediated cell cycle arrest.
- OASIS-induced p21 expression is independent of p53.
- OASIS exhibits distinct yet complementary roles to p53 in cell cycle control.
Conclusions:
- ER-resident transcription factor OASIS is a novel regulator of cell cycle arrest.
- OASIS functions independently of the p53 pathway in DNA damage response.
- OASIS dysregulation is linked to tumorigenesis, highlighting its potential as a tumor suppressor and therapeutic target.
Keywords:
DNA damageOASISastrocytecell cycle arrestglioblastomamethylationp21p53tumor suppressortumorigenesisMore Related Videos
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