Cell adhesion or cell to cell contact is imperative for the survival of human cells under protein-damaging and stressful conditions, according to a study. It was also revealed that cancer cells become more vulnerable to anti-cancer drugs when their cell adhesion is impaired.
The study was led by Lea Sistonen, Professor in Cell and Molecular Biology at Abo Akademi University was published in the Cell Reports journal.
Sistonen said: "Our results show, for the first time, that the contacts between cells, known as cell adhesion, are essential for cells to survive stress. The findings also suggest that impaired cell adhesion may sensitize cancer cells to drugs that damage cell proteins and cause stress."
The research project focused on heat shock factor 2 (HSF2), a specialized gene-regulating protein, and its impact on cells' capacity to survive protein-damaging stress which is usually caused by, high temperatures, virus infections and certain anti-cancer medications.The results revealed that HSF2 contributes to protecting cells against stress by regulating those genes that mediate cell adhesion contacts.
The findings were obtained by studying how cancer cells respond to some commonly used anticancer medicines, among other things. Cancer cells with compromised adhesion interactions in drug treatment were slightly less active than those with stable adhesion to the cells.
"Cell-to-cell contacts are essential for normal tissue functioning and mechanisms. Cancer cells are known to utilize these contacts to form aggressive tumours and metastases. Our results show, indeed, that cancer cells become more vulnerable to drug treatment when their cell contacts are weakened", said Sistonen.
Cell adhesion contact is mediated by proteins known as cadherins which are used as the source of message chains that regulate cell death. However, further research is needed to understand the molecular foundation for these processes. Individual differences in these cell processes can partly explain why some drugs work for some, but not for others, he further explained.
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