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Exploring Caspase Mutations and Post-Translational Modification by Molecular Modeling Approaches
Published on: October 13, 2022
Caspase-2: the reinvented enzyme
M Olsson1, J Forsberg1, B Zhivotovsky2
1Division of Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Abstract:
On the basis of evidences that caspase-2 gene targeting in several generated mouse models accelerates tumor formation, this enzyme was recently implicated in tumor suppression. The observed function, however, compels other molecular perturbations harboring tumorigenic properties. Therefore, the question remains as to whether or not caspase-2 can be considered a true tumor suppressor? The traditional view of caspase-2 being vital for the apoptotic response to induced cell stress in some systems is in line with these findings. Yet, caspase-2 has also been associated with other processes which equally might interfere with tumorigenic potential, including the oxidative stress response, aging and genome surveillance. By different mechanisms, this enzyme has been proposed to function as a checkpoint regulator in the cell cycle. Together, these data indicate that caspase-2 is a highly versatile factor, a view that is contrasted by the alternative explanation where the enzyme harbors a mechanism affecting a discrete process, which in turn is functionally connected to other cell systems. In any case, it is clear that the general view of caspase-2 as a protein mainly involved in apoptotic cell death is shattered. Hence, we wish to discuss the perspectives of recent achievements in caspase-2-related research.
Insights
Caspase-2
Area of Science:
- Molecular Biology
- Oncology
- Cellular Biology
Background:
- Caspase-2 gene targeting in mouse models accelerates tumor formation, implicating it in tumor suppression.
- This observed function raises questions about caspase-2's role, considering potential concurrent tumorigenic molecular perturbations.
Purpose of the Study:
- To critically evaluate whether caspase-2 can be definitively classified as a tumor suppressor.
- To explore the multifaceted roles of caspase-2 beyond its traditional association with apoptosis.
Main Methods:
- Review of existing evidence on caspase-2 function in tumor formation and suppression.
- Analysis of caspase-2's involvement in oxidative stress response, aging, and genome surveillance.
- Examination of caspase-2's proposed role as a cell cycle checkpoint regulator.
Main Results:
- Caspase-2's function extends beyond apoptosis, involving processes like oxidative stress response, aging, and genome surveillance.
- The enzyme acts as a cell cycle checkpoint regulator through various mechanisms.
- Evidence suggests caspase-2 is a versatile factor with complex roles in tumorigenesis.
Conclusions:
- The traditional view of caspase-2 solely mediating apoptotic cell death is challenged.
- Caspase-2's diverse functions indicate a complex interplay with cellular processes relevant to cancer.
- Further research is needed to fully elucidate caspase-2's precise mechanisms and its net effect on tumor suppression.
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