Bacterial survival hinges on resistance, persistence, or tolerance when confronted with antibiotic therapy. Similarly, cancer cells have resistance and persistence strategies to counter chemotherapy, though whether drug-triggered tolerance exists has been unclear.

 

In a new publication in Nature Communications, Punzi et al. propose that cancer cells do possess a tolerance mechanism that relies on autophagy activation and DNA damage repair pathway enhancement (1). Interestingly, extended drug exposure elicits transition to persistence characterized by a reversal in DNA repair pathway activity. This effect is mediated by a PINK1/HNF4A-dependent mechanism involving chromatin compaction and transcriptional silencing. The authors suggest that therapeutic inhibition of tolerance, in combination with standard antineoplastic regimens, could potentially improve patient outcomes.

 

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Reference:

Nat. Commun. 2025 Feb 3;16(1):1291. doi: 10.1038/s41467-024-54728-7