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Published on: April 12, 2024
The expression of SPARC in human tumors is consistent with its role during cell competition
Evgeniya Petrova1, Davide Soldini, Eduardo Moreno
1Molecular Oncology Programme; Spanish National Cancer Centre (CNIO); Madrid, Spain.
Abstract:
In Drosophila, the elimination of viable but suboptimal cells is mediated by cell competition, ensuring that these cells do not accumulate during development. In addition, certain genes such as the Drosophila homologue of human c-myc (dmyc) are able to transform cells into supercompetitors, which eliminate neighboring wild-type cells by apoptosis and overproliferate leaving total cell numbers unchanged. We have recently identified Drosophila SPARC as an early marker transcriptionally upregulated in loser cells that provides a transient protection by inhibiting caspase activation in outcompeted cells. Here, we explore whether the expression of SPARC in human tumors is consistent with a role for cell competition during human cancer and find that, consistent with the existence of competitive interactions between cancer and normal cells, SPARC is upregulated at the tumor-host boundaries in several types of human cancer.
Insights
Cell competition eliminates suboptimal cells during development. In human cancers, SPARC is upregulated at tumor boundaries, suggesting competitive interactions between cancer and normal cells.
Area of Science:
- Developmental Biology
- Cancer Biology
- Cellular Interactions
Background:
- Cell competition is a mechanism in Drosophila development where suboptimal cells are eliminated.
- Genes like dmyc can induce supercompetitor cells that eliminate neighbors via apoptosis.
- Drosophila SPARC is identified as a marker in loser cells, inhibiting apoptosis.
Purpose of the Study:
- To investigate if SPARC expression in human tumors reflects a role for cell competition in cancer.
- To determine if competitive interactions occur between cancer cells and normal host cells.
Main Methods:
- Analysis of SPARC expression in human tumor samples.
- Comparison of SPARC expression patterns at tumor-host boundaries.
Main Results:
- SPARC is upregulated at the tumor-host boundaries in several human cancer types.
- This upregulation is consistent with competitive interactions between cancer and normal cells.
Conclusions:
- SPARC expression in human tumors supports the hypothesis of cell competition occurring in cancer.
- Cell competition may play a role in the dynamics of tumor-host interactions.
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