Protein hSpindly Linked to Cancer Drug Resistance, Study Finds

A newly identified role for the protein hSpindly helps explain why some tumour cells resist antimitotic drugs that are designed to block their division. The finding, published in iScience and led by the University of Sevilla and the Cancer Research Center of Salamanca, reveals a molecular switch that could serve as a biomarker or future drug target. Source: elconfidencial, infobae

The mechanism

hSpindly is part of the spindle assembly checkpoint (SAC), a system that ensures chromosomes are correctly distributed during cell division. The study shows that when cells are treated with antimitotic drugs, hSpindly's dynamic behaviour—controlled by phosphorylation at the amino acid threonine 552—determines whether the SAC remains active, ultimately influencing whether the cell dies or survives. Source: elconfidencial Blocking phosphorylation (via a T552A mutation) makes hSpindly less able to recruit Mad2, weakening the checkpoint and allowing cells to escape drug action. Source: infobae

Implications

Researcher Nuria Ferrándiz noted that hSpindly was previously seen as merely a structural adapter, but these results show it directly participates in SAC activation. Source: elconfidencial The study used human cell lines without animal models. Source: infobae This opens avenues for using hSpindly as a biomarker for patient response or designing drugs that target its regulatory switch. Source: elconfidencial