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Cell cycle regulation and apoptosis
1Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, Ohio 45267-0576, USA.
Abstract:
Tissue homeostasis requires a balance between cell proliferation and death. Apoptosis and proliferation are linked by cell cycle regulators, and apoptotic stimuli affect both cell proliferation and death. Glucocorticoids induce G1 arrest and apoptosis in transformed lymphoid cells. Decreased expression of the cell cycle components c-myc and cyclin D3 is essential for glucocorticoid-induced growth arrest and death in dividing cells. Other G1 regulators, such as p53, pRb, and E2F, have also been implicated in apoptosis. Mice lacking either p53 or E2F display aberrant cell proliferation and tumor formation, suggesting that these proteins are involved in the elimination of abnormal cells through apoptosis. In contrast, pRb induces G1 arrest and suppresses apoptosis in cultured cells. Mice that lack pRb are nonviable and show ectopic mitosis and massive cell death, suggesting that pRb is an apoptotic suppressor. Further analysis of common components of apoptotic and cell cycle machinery may provide insight into the coordinated regulation of these antagonistic processes.
Insights
Cell cycle regulators like p53 and pRb are crucial for maintaining tissue homeostasis by balancing cell proliferation and apoptosis. Understanding these links offers insights into coordinated regulation of cell death and growth.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Tissue homeostasis depends on the balance between cell proliferation and programmed cell death (apoptosis).
- Cell cycle regulators are key mediators linking apoptotic stimuli to both cell proliferation and death.
- Glucocorticoids are known to induce G1 cell cycle arrest and apoptosis in lymphoid cells.
Purpose of the Study:
- To investigate the role of cell cycle regulators in apoptosis and tissue homeostasis.
- To elucidate the mechanisms by which glucocorticoids induce growth arrest and death in lymphoid cells.
- To explore the interplay between cell cycle machinery and apoptotic pathways.
Main Methods:
- Analysis of cell cycle components (e.g., c-myc, cyclin D3, p53, pRb, E2F) in response to apoptotic stimuli.
- Examination of knockout mouse models lacking specific cell cycle regulators (p53, E2F, pRb).
- In vitro studies on cultured cells to assess the effects of pRb on apoptosis.
Main Results:
- Decreased expression of c-myc and cyclin D3 is essential for glucocorticoid-induced growth arrest and apoptosis.
- Loss of p53 or E2F in mice leads to abnormal proliferation and tumor formation, indicating their role in eliminating aberrant cells.
- pRb functions as an apoptotic suppressor, inducing G1 arrest and preventing cell death; its absence results in non-viability and massive cell death.
Conclusions:
- Cell cycle regulators play critical roles in apoptosis and are integral to maintaining tissue homeostasis.
- The coordinated regulation of cell proliferation and apoptosis involves shared components of cell cycle and apoptotic machinery.
- Further research into these common components can illuminate the intricate control of these opposing cellular processes.