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Using CRISPR/Cas9 Gene Editing to Investigate the Oncogenic Activity of Mutant Calreticulin in Cytokine Dependent Hematopoietic Cells
Published on: January 5, 2018
Enhanced calreticulin expression triggers apoptosis in the MCF-7 cell line
Shibily Prathyuman1, Sudha Sellappa, Shyn Joseph
1Department of Biotechnology, Karpagam University, Coimbatore, Tamilnadu, India.
Abstract:
Calreticulin, since its discovery as a ubiquitous protein of endoplasmic reticulum, has become recognized as a multifunctional luminal resident protein affecting many cellular functions ranging from development to death of a cell. However its role in cancer and significance for therapy remains to be clarified. Here to examine its effects, the calreticulin gene was over expressed in MCF-7 human breast cancer cell lines and influence on apoptosis was examined through an MTT assay. Upon culture in a suitable medium, cells transfected with the calreticulin gene were significantly more susceptible to apoptosis compared to controls. These findings therefore render a novel mechanism by which cancerous cells can be triggered to undergo death by upregulation of a protein resident in the lumen of the endoplasmic reticulum.
Insights
Overexpressing calreticulin in breast cancer cells increased apoptosis. This suggests a new way to trigger cancer cell death by upregulating this endoplasmic reticulum protein.
Area of Science:
- Cell Biology
- Molecular Biology
- Oncology
Background:
- Calreticulin is a multifunctional protein found in the endoplasmic reticulum.
- Its role in cancer development and therapeutic potential requires further investigation.
Purpose of the Study:
- To investigate the effect of calreticulin gene overexpression on apoptosis in MCF-7 human breast cancer cells.
- To explore a novel mechanism for inducing cancer cell death.
Main Methods:
- Overexpression of the calreticulin gene in MCF-7 cells.
- Assessment of apoptosis using an MTT assay.
Main Results:
- Cells with overexpressed calreticulin showed significantly higher susceptibility to apoptosis compared to control cells.
- Upregulation of calreticulin promotes programmed cell death in cancer cells.
Conclusions:
- Calreticulin overexpression can trigger apoptosis in human breast cancer cells.
- Targeting calreticulin presents a potential therapeutic strategy for cancer treatment.
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