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University of Seville study identifies protein key to cancer treatment resistance

Research reveals how the hSpindly protein influences the effectiveness of anti-mitotic chemotherapy drugs.

Generic image of a scientific research laboratory.
IA

Generic image of a scientific research laboratory.

A research team from the University of Seville and the Cancer Research Center has determined the function of the hSpindly protein in cell division and its impact on chemotherapy.

The study, published in the journal iScience, analyzes how tumor cells manage to evade the effect of anti-mitotic drugs. These medications are designed to block cell division and cause the death of cancer cells, but their effectiveness decreases when cells manage to overcome this blockade.
The hSpindly protein is located in the fibrous corona of the chromosome, facilitating its attachment to microtubules during mitosis. According to experts, this protein acts as a dynamic component that participates in the activation of the spindle assembly checkpoint, the system responsible for monitoring the correct distribution of chromosomes.
The research has identified that a specific modification in the amino acid threonine 552 allows the protein to act as a precise switch. When this point is not phosphorylated, the protein loses its ability to attract other regulatory molecules, such as Mad2, altering the control signal and allowing tumor cells to survive treatment.
This finding opens the door to considering hSpindly as a potential biomarker or a future therapeutic target. The research was conducted exclusively using human cell lines cultured in the laboratory, without the use of animal models.