Mitochondrial dysfunction induced by a SH2 domain-targeting STAT3 inhibitor leads to metabolic synthetic lethality in cancer cells
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Significance: The transcription factor STAT3 is involved in multiple oncogenic signaling pathways and is an attractive therapeutic target. This study shows that a potent inhibitor of STAT3 interferes with mitochondrial activity and protein homeostasis, leading to a synthetic lethality effect in glucose-depleted cancer cells. These findings provide a rationale for novel strategies based on the use of STAT3 inhibitors for cancer treatment.
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STAT3 forms proteotoxic aggregates in mitochondria when tumor cells are treated with OPB-51602, STA21, or WP1066.
“For instance, it has been reported that STAT3 forms proteotoxic aggregates in mitochondria when tumor cells are treated with OPB-51602, STA21, or WP1066 (Genini et al., 2017).”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Genini et al., 2017
The sections “STAT3 Forms Proteotoxic Aggregates in the Presence of OPB-51602” and “Mitochondrial Dysfunction and Proteotoxic Aggregate Formation” report STAT3 aggregates after treatment with OPB-51602 and other inhibitors, including STA21 and WP1066. But the claimed location is wrong: fractionation found STAT3 depleted from mitochondria after OPB-51602 treatment and shifted into an insoluble protein fraction, not aggregated in mitochondria. No page numbers are available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredToxicities observed in Phase I/II studies of OPB-31121 that halted its further development resulted from its targeting of mtSTAT3.
“The toxicities observed in Phase I/II studies of OPB-31121 that halted its further development resulted from its targeting of mtSTAT3 (Genini et al., 2017).”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Genini et al., 2017
In the section “OPB-51602 Inhibits STAT3 by Binding to the SH2D” (page not supplied), the paper includes OPB-31121 in a cell-based mitochondrial membrane-potential assay, but establishes mSTAT3-dependent cytotoxicity specifically for OPB-51602. The References list Phase I studies of OPB-31121; our copy does not establish that mtSTAT3 targeting caused toxicities in those patients or that toxicities halted the drug’s development. (LLM, conf=0.83)
Experimental — accuracy not yet measuredStudies performed in parallel with other STAT3 inhibitors previously shown to target mtSTAT3 were confirmatory.
“Our studies showed that TTI-101 did not affect mitochondrial ATP generation or oxygen consumption, whereas studies performed in parallel with other STAT3 inhibitors previously shown to target mtSTAT3 (Genini et al., 2017) were confirmatory (data not shown).”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Genini et al., 2017
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- Authors
- Genini, D., Brambilla, L., Laurini, E., Merulla, J., Civenni, G., Pandit, S., D'Antuono, R., Perez, L., Levy, D. E., Pricl, S., Carbone, G. M., & Catapano, C. V.
- Affiliations
- Institute of Oncology Research (CH)
- University of Trieste (IT)
- Institute for Research in Biomedicine, Università della Svizzera Italiana, 6500 Bellinzona, Switzerland;
- Institute for Research in Biomedicine (CH)
- New York University (US)
- Corresponding author
- Catapano, Carlo V.
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2017-06-05
- Volume
- 114
- Issue
- 25
- Pages
- E4924-E4933
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC5488915
- OpenAlex
- W2624425423
- Cited by
- 106
- References
- 68
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 9 · 2023: 8 · 2022: 10 · 2021: 21 · 2020: 17 · 2019: 10 · 2018: 14 · 2017: 1
- FWCI
- 5.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- ArTS Archivio della ricerca di Trieste (University of Trieste https://www.units.it/) (submittedVersion, other-oa)
- reroDoc Digital Library (submittedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- National Institutes of Health (STAT3)
- National Institute of Allergy and Infectious Diseases (R01AI028900)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- STAT3, mitochondrial STAT3, SH2 domain inhibitors, mitochondrial dysfunction, synthetic lethality, cancer metabolism, glucose deprivation, cancer stem cells, cell death, cancer therapy
- MeSH terms
- Synthetic Lethal Mutations, Animals, Humans, Male, Mice, Nude, Mitochondria, Neoplasms, Cell Death, src Homology Domains, Cell Line, Tumor, STAT3 Transcription Factor, Mice
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