Nanoengineered Disruption of Heat Shock Protein 90 Targets Drug-Induced Resistance and Relieves Natural Killer Cell Suppression in Breast Cancer.
Animals
Antineoplastic Agents, Immunological
/ chemistry
Breast Neoplasms
/ drug therapy
Cell Line, Tumor
Cholesterol
/ chemistry
Docetaxel
/ administration & dosage
Drug Delivery Systems
Drug Liberation
Drug Resistance, Neoplasm
Female
HSP90 Heat-Shock Proteins
/ antagonists & inhibitors
Humans
Killer Cells, Natural
/ drug effects
Macrolides
/ chemistry
Mice, Inbred BALB C
Molecular Targeted Therapy
/ methods
Nanoparticles
/ chemistry
Triple Negative Breast Neoplasms
/ drug therapy
Tumor Microenvironment
/ drug effects
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
01 12 2020
01 12 2020
Historique:
received:
29
12
2019
revised:
16
08
2020
accepted:
09
10
2020
pubmed:
21
10
2020
medline:
6
3
2021
entrez:
20
10
2020
Statut:
ppublish
Résumé
Drug-induced resistance, or tolerance, is an emerging yet poorly understood failure of anticancer therapy. The interplay between drug-tolerant cancer cells and innate immunity within the tumor, the consequence on tumor growth, and therapeutic strategies to address these challenges remain undescribed. Here, we elucidate the role of taxane-induced resistance on natural killer (NK) cell tumor immunity in triple-negative breast cancer (TNBC) and the design of spatiotemporally controlled nanomedicines, which boost therapeutic efficacy and invigorate "disabled" NK cells. Drug tolerance limited NK cell immune surveillance via drug-induced depletion of the NK-activating ligand receptor axis, NK group 2 member D, and MHC class I polypeptide-related sequence A, B. Systems biology supported by empirical evidence revealed the heat shock protein 90 (Hsp90) simultaneously controls immune surveillance and persistence of drug-treated tumor cells. On the basis of this evidence, we engineered a "chimeric" nanotherapeutic tool comprising taxanes and a cholesterol-tethered Hsp90 inhibitor, radicicol, which targets the tumor, reduces tolerance, and optimally reprimes NK cells via prolonged induction of NK-activating ligand receptors via temporal control of drug release
Identifiants
pubmed: 33077554
pii: 0008-5472.CAN-19-4036
doi: 10.1158/0008-5472.CAN-19-4036
pmc: PMC7718318
mid: NIHMS1638223
doi:
Substances chimiques
Antineoplastic Agents, Immunological
0
HSP90 Heat-Shock Proteins
0
Macrolides
0
Docetaxel
15H5577CQD
Cholesterol
97C5T2UQ7J
monorden
I60EH8GECX
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
5355-5366Subventions
Organisme : NCI NIH HHS
ID : U01 CA214411
Pays : United States
Informations de copyright
©2020 American Association for Cancer Research.
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