Small-molecule RNA therapeutics to target prostate cancer
Open accessAbstract
Tuning protein expression by targeting RNA structure using small molecules is an unexplored avenue for cancer treatment. To understand whether this vulnerability could be therapeutically targeted in the most lethal form of prostate cancer, castration-resistant prostate cancer (CRPC), we use a clinical small molecule, zotatifin, that targets the RNA helicase and translation factor eukaryotic initiation factor 4A (eIF4A). Zotatifin represses tumorigenesis in patient-derived and xenograft models and prolonged survival in vivo alongside hormone therapy. Genome-wide transcriptome, translatome, and proteomic analysis reveals two important translational targets: androgen receptor (AR), a key oncogene in CRPC, and hypoxia-inducible factor 1A (HIF1A), an essential cancer modulator in hypoxia. We solve the structure of the 5' UTRs of these oncogenic mRNAs and strikingly observe complex structural remodeling of these select mRNAs by this small molecule. Remarkably, tumors treated with zotatifin become more sensitive to anti-androgen therapy and radiotherapy. Therefore, "translatome therapy" provides additional strategies to treat the deadliest cancers.
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eIF4A inhibitors target both isoforms, suppress translation of key oncogenes, and have demonstrated antitumor activity in a variety of cancers.
“eIF4A inhibitors, which target both isoforms, suppress translation of key oncogenes and have demonstrated antitumor activity in a variety of cancers (15, 17, 19–22).”
From Targeting eIF4A-dependent translation in genetically complex sarcoma (2026) · cites this paper as [22]
The Results section on eIF4A inhibition reports that zotatifin reduced prostate-tumor growth and prolonged survival in mouse models; the Discussion links its anticancer effect to reduced translation of the cancer drivers AR and HIF1A. Our copy does not establish that eIF4A inhibitors target both eIF4A isoforms or demonstrate antitumor activity across a variety of cancer types. Its reference to inhibiting 'both isoforms' concerns AR, not eIF4A. Page numbers are unavailable in our copy. (LLM, conf=0.87)
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- Authors
- Kuzuoglu-Ozturk, D., Nguyen, H. G., Xue, L., Figueredo, E., Subramanyam, V., Liu, I., Bonitto, K., Noronha, A., Dabrowska, A., Cowan, J. E., Oses-Prieto, J. A., Burlingame, A. L., Worland, S. T., Carroll, P. R., & Ruggero, D.
- Affiliations
- University of California, San Francisco (US)
- eFFECTOR Therapeutics (United States) (US)
- Corresponding author
- Nguyen, Hao G.
- Ruggero, Davide
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2025-05
- Volume
- 43
- Issue
- 5
- Pages
- 841-855.e8
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC12124822
- OpenAlex
- W4408660129
- Cited by
- 24
- References
- 60
- Citations by year
- 2026: 14 · 2025: 10
- FWCI
- 15.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 376 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (publishedVersion)
- Sabanci University (acceptedVersion)
- Funders
- American Cancer Society (P50CA275741, RP-19-181-01-RMC)
- US Department of Defense (HT9425-24-1-0070)
- Prostate Cancer Foundation
- Portland Community Fund (R01CA235741)
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- National Institutes of Health National Cancer Institute (R35CA242986)
- National Institutes of Health
- University of California, San Francisco
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA modifications and cancer
- Keywords
- castration-resistant prostate cancer, eIF4A, RNA helicase, translatome, androgen receptor, HIF1A, antiandrogen therapy, radiosensitivity, hormone therapy
- MeSH terms
- Animals, Humans, Male, Prostatic Neoplasms, Receptors, Androgen, RNA, Messenger, Thiohydantoins, Gene Expression Regulation, Neoplastic, 5' Untranslated Regions, Xenograft Model Antitumor Assays, Eukaryotic Initiation Factor-4A, Cell Line, Tumor, Mice, Hypoxia-Inducible Factor 1, alpha Subunit, Prostatic Neoplasms, Castration-Resistant
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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