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Updated: Aug 10, 2026
Adenofection: A Method for Studying the Role of Molecular Chaperones in Cellular Morphodynamics by Depletion-Rescue Experiments
Published on: September 16, 2016
Induction of polyploidy in adenovirus E1-transformed cells by the mitotic inhibitor colcemid
O Kranenburg1, A J Van der Eb, A Zantema
1Sylvius Laboratory, Department of Molecular Carcinogenesis, Leiden University, The Netherlands.
Abstract:
Adenovirus-transformed cells were tested for their ability to synthesize DNA in the presence of cell cycle inhibitory drugs. We show that transformed cells are completely resistant to the mitotic inhibitor colcemid, partly resistant to lovastatin, mimosine, aphidicolin and genistein but not to hydroxyurea or thymidine. When treated with colcemid, AdE1-transformed cells continue to synthesize DNA but do not divide and, therefore, become highly polyploid. This effect is dependent on the presence of both E1A and E1B.
Insights
Adenovirus-transformed cells resist cell cycle inhibitors like colcemid, continuing DNA synthesis without dividing. This leads to polyploidy, an effect requiring both E1A and E1B viral proteins.
Area of Science:
- Cell biology
- Virology
- Molecular biology
Background:
- Cell cycle regulation is crucial for normal cell function.
- Viral oncogenes can disrupt normal cellular processes, including cell cycle control.
Purpose of the Study:
- To investigate the DNA synthesis capabilities of adenovirus-transformed cells under cell cycle arrest.
- To determine the resistance profile of these cells against various cell cycle inhibitory drugs.
Main Methods:
- Adenovirus-transformed cells were treated with a panel of cell cycle inhibitors.
- DNA synthesis was measured in treated cells.
- Cellular ploidy was assessed after treatment with colcemid.
Main Results:
- Transformed cells exhibited complete resistance to colcemid and partial resistance to lovastatin, mimosine, aphidicolin, and genistein.
- Hydroxyurea and thymidine did not inhibit DNA synthesis in these cells.
- Colcemid treatment induced high polyploidy in AdE1-transformed cells, dependent on E1A and E1B expression.
Conclusions:
- Adenovirus E1A and E1B proteins confer resistance to specific cell cycle inhibitors, enabling continued DNA synthesis.
- This resistance leads to polyploidization, highlighting a mechanism by which viral oncogenes disrupt cell cycle checkpoints.
