AI Article Synopsis
- ALG-2 is a calcium-binding protein that is overexpressed in various cancers; its downregulation may lead to cancer cell death.
- Research indicates that ALG-2 is crucial for membrane repair and helps cells withstand damage, as seen in experiments with DT-40 cells where the loss of ALG-2 made them more sensitive to damage from electroporation.
- The study suggests that enhancing ALG-2 could provide protective effects against cell death, making it a potential new target for cancer therapies that involve damaging cell membranes.
Article Abstract
The calcium binding protein ALG-2 is upregulated in several types of cancerous tissues and cancer cell death may be a consequence of ALG-2 downregulation. Novel research suggests that ALG-2 is involved in membrane repair mechanisms, in line with several published studies linking ALG-2 to processes of membrane remodeling and transport, which may contribute to the fitness of cells or protect them from damage. To investigate the involvement of ALG-2 in cell recovery after membrane damage we disrupted the PDCD6 gene encoding the ALG-2 protein in DT-40 cells and exposed them to electroporation. ALG-2 knock-out cells were more sensitive to electroporation as compared to wild type cells. This phenotype could be reversed by reestablishing ALG-2 expression confirming that ALG-2 plays an important role in cell recovery after plasma membrane damage. We found that overexpression of wild type ALG-2 but not a mutated form unable to bind Ca2+ partially protected HeLa cells from digitonin-induced cell death. Further, we were able to inhibit the cell protective function of ALG-2 after digitonin treatment by adding a peptide with the ALG-2 binding sequence of ALIX, which has been proposed to serve as the ALG-2 downstream target in a number of processes including cell membrane repair. Our results suggest that ALG-2 may serve as a novel therapeutic target in combination with membrane damaging interventions.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6150531 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0204520 | PLOS |
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