A cisplatin conjugate with tumor cell specificity exhibits antitumor effects in renal cancer models.


Journal

BMC cancer
ISSN: 1471-2407
Titre abrégé: BMC Cancer
Pays: England
ID NLM: 100967800

Informations de publication

Date de publication:
02 Jun 2023
Historique:
received: 31 10 2022
accepted: 24 04 2023
medline: 5 6 2023
pubmed: 3 6 2023
entrez: 2 6 2023
Statut: epublish

Résumé

Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer and is notorious for its resistance to both chemotherapy and small-molecule inhibitor targeted therapies. Subcellular targeted cancer therapy may thwart the resistance to produce a substantial effect. We tested whether the resistance can be circumvented by subcellular targeted cancer therapy with DZ-CIS, which is a chemical conjugate of the tumor-cell specific heptamethine carbocyanine dye (HMCD) with cisplatin (CIS), a chemotherapeutic drug with limited use in ccRCC treatment because of frequent renal toxicity. DZ-CIS displayed cytocidal effects on Caki-1, 786-O, ACHN, and SN12C human ccRCC cell lines and mouse Renca cells in a dose-dependent manner and inhibited ACHN and Renca tumor formation in experimental mouse models. Noticeably, in tumor-bearing mice, repeated DZ-CIS use did not cause renal toxicity, in contrast to the CIS-treated control animals. In ccRCC tumors, DZ-CIS treatment inhibited proliferation markers but induced cell death marker levels. In addition, DZ-CIS at half maximal inhibitory concentration (IC50) sensitized Caki-1 cells to small-molecule mTOR inhibitors. Mechanistically, DZ-CIS selectively accumulated in ccRCC cells' subcellular organelles, where it damages the structure and function of mitochondria, leading to cytochrome C release, caspase activation, and apoptotic cancer cell death. Results from this study strongly suggest DZ-CIS be tested as a safe and effective subcellular targeted cancer therapy.

Sections du résumé

BACKGROUND BACKGROUND
Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer and is notorious for its resistance to both chemotherapy and small-molecule inhibitor targeted therapies. Subcellular targeted cancer therapy may thwart the resistance to produce a substantial effect.
METHODS METHODS
We tested whether the resistance can be circumvented by subcellular targeted cancer therapy with DZ-CIS, which is a chemical conjugate of the tumor-cell specific heptamethine carbocyanine dye (HMCD) with cisplatin (CIS), a chemotherapeutic drug with limited use in ccRCC treatment because of frequent renal toxicity.
RESULTS RESULTS
DZ-CIS displayed cytocidal effects on Caki-1, 786-O, ACHN, and SN12C human ccRCC cell lines and mouse Renca cells in a dose-dependent manner and inhibited ACHN and Renca tumor formation in experimental mouse models. Noticeably, in tumor-bearing mice, repeated DZ-CIS use did not cause renal toxicity, in contrast to the CIS-treated control animals. In ccRCC tumors, DZ-CIS treatment inhibited proliferation markers but induced cell death marker levels. In addition, DZ-CIS at half maximal inhibitory concentration (IC50) sensitized Caki-1 cells to small-molecule mTOR inhibitors. Mechanistically, DZ-CIS selectively accumulated in ccRCC cells' subcellular organelles, where it damages the structure and function of mitochondria, leading to cytochrome C release, caspase activation, and apoptotic cancer cell death.
CONCLUSIONS CONCLUSIONS
Results from this study strongly suggest DZ-CIS be tested as a safe and effective subcellular targeted cancer therapy.

Identifiants

pubmed: 37268911
doi: 10.1186/s12885-023-10878-3
pii: 10.1186/s12885-023-10878-3
pmc: PMC10236852
doi:

Substances chimiques

Cisplatin Q20Q21Q62J

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

499

Subventions

Organisme : NCI NIH HHS
ID : R21 CA256419
Pays : United States
Organisme : NIH HHS
ID : R21CA256419
Pays : United States

Informations de copyright

© 2023. The Author(s).

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Auteurs

Stefan Mrdenovic (S)

Division of Hematology, Department of Internal Medicine, University Hospital Osijek, Osijek, Croatia.
Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Department of Internal Medicine, Family Medicine and History of Medicine, Faculty of Medicine, J. J. Strossmayer University of Osijek, Osijek, Croatia.

Yanping Wang (Y)

Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Lijuan Yin (L)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Gina Chia-Yi Chu (GC)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Yan Ou (Y)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Michael S Lewis (MS)

Departments of Pathology, Cedars-Sinai Medical Center and the VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA.

Marija Heffer (M)

Department of Medical Biology and Genetics, Faculty of Medicine, J. J. Strossmayer University of Osijek, Osijek, Croatia.

Edwin M Posadas (EM)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Haiyen E Zhau (HE)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Leland W K Chung (LWK)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Mouad Edderkaoui (M)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Stephen J Pandol (SJ)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Ruoxiang Wang (R)

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Departments of Pathology, Cedars-Sinai Medical Center and the VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA.

Yi Zhang (Y)

Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Davis 3059, 90048, Los Angeles, CA, USA. yi.zhang@cshs.org.

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Classifications MeSH