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Updated: Oct 31, 2025
12:49
Mutagenesis and Analysis of Genetic Mutations in the GC-rich KISS1 Receptor Sequence Identified in Humans with Reproductive Disorders
Published on: September 4, 2011
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Ki-67 gene expression
Sigrid Uxa1, Paola Castillo-Binder1, Robin Kohler1
1Molecular Oncology, Medical School, University of Leipzig, Leipzig, Germany.
Cell Death and Differentiation
|June 29, 2021
Summary
The MKI67 gene, which codes for the cancer marker Ki-67, is tightly regulated during the cell cycle. Its expression peaks in G2/M phases, influenced by transcription factors and tumor suppressors like p53.
Area of Science:
- Molecular Biology
- Cell Cycle Regulation
- Cancer Biology
Background:
- Ki-67 (encoded by MKI67) is a crucial cancer marker.
- Understanding MKI67 gene expression control is vital for cancer research.
Purpose of the Study:
- To elucidate the regulatory mechanisms of MKI67 gene expression during the cell cycle.
- To investigate the role of transcription factors and tumor suppressors in MKI67 regulation.
Main Methods:
- Analysis of MKI67 promoter elements (CHR, CDE).
- Study of transcription factor binding (DREAM, B-MYB-MuvB, FOXM1-MuvB).
- Utilized knockout cell models and knockdown experiments.
Main Results:
- MKI67 expression peaks in G2/M phase, driven by B-MYB-MuvB and FOXM1-MuvB binding.
- DREAM repressor complexes downregulate MKI67 in G0/G1.
- RB tumor suppressor cooperates with DREAM/MuvB.
- p53 tumor suppressor indirectly represses MKI67 via p21/CDKN1A.
Conclusions:
- A model for cell cycle-dependent MKI67 transcription involving DREAM, MuvB complexes, and RB is proposed.
- p53 activation and DNA damage induce MKI67 repression through p21/CDKN1A.
- These findings provide insights into MKI67 regulation in normal and cancer cells.
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