C‑terminal HSP90 inhibitor NCT‑58 impairs the cancer stem‑like phenotype and enhances chemotherapy efficacy in TNBC.

ABSTRACT: Treatment options for triple‑negative breast cancer (TNBC) are limited because they typically harbor a high cancer stem‑like population and exhibit a relatively aggressive metastatic phenotype. Heat shock protein 90 (HSP90), a molecular chaperone that regulates diverse oncogenic client proteins, has emerged as a compelling therapeutic target owing to its involvement in key tumor‑promoting processes, such as uncontrolled proliferation, angiogenesis and metastasis. Owing to the undesirable induction of a compensatory heat shock response (HSR) and systemic toxicity, classical N‑terminal inhibitors of HSP90 have failed in clinical trials. The impact of a rationally designed novel inhibitor of the HSP90 C‑terminus in TNBC cells was investigated. NCT‑58 eliminates rapidly proliferating tumor cel

SUBMITTER: Jung E 

PROVIDER: S-EPMC12635604 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature