FBXO44 promotes DNA replication-coupled repetitive element silencing in cancer cells
Open accessAbstract
Repetitive elements (REs) compose ∼50% of the human genome and are normally transcriptionally silenced, although the mechanism has remained elusive. Through an RNAi screen, we identified FBXO44 as an essential repressor of REs in cancer cells. FBXO44 bound H3K9me3-modified nucleosomes at the replication fork and recruited SUV39H1, CRL4, and Mi-2/NuRD to transcriptionally silence REs post-DNA replication. FBXO44/SUV39H1 inhibition reactivated REs, leading to DNA replication stress and stimulation of MAVS/STING antiviral pathways and interferon (IFN) signaling in cancer cells to promote decreased tumorigenicity, increased immunogenicity, and enhanced immunotherapy response. FBXO44 expression inversely correlated with replication stress, antiviral pathways, IFN signaling, and cytotoxic T cell infiltration in human cancers, while a FBXO44-immune gene signature correlated with improved immunotherapy response in cancer patients. FBXO44/SUV39H1 were dispensable in normal cells. Collectively, FBXO44/SUV39H1 are crucial repressors of RE transcription, and their inhibition selectively induces DNA replication stress and viral mimicry in cancer cells.
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H3K9me3 produced by SUV39H1, SUV39H2, and SETDB1 methyltransferases accumulates in repetitive sequence regions in breast cancer cells.
“Our previous research revealed that H3K9me3, produced by SUV39H1, SUV39H2, and SETDB1 methyltransferases, accumulates in repetitive sequence regions in breast cancer cells3.”
From Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity (2025) · cites this paper as [3]
The Results section (‘FBXO44 is essential for H3K9me3-mediated transcriptional silencing of REs in cancer cells’; page unavailable) reports H3K9me3 at repetitive elements, and the Discussion identifies SUV39H1 as part of the complex that restores it. The Introduction lists SUV39H2 and SETDB1 as enzymes that can mediate H3K9me3 generally, but the cited passages do not establish that all three produce the modification at repetitive elements in breast cancer cells. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSUV39H1 targeting activates interferon signaling pathways in breast cancer cells, leading to tumor growth arrest and improved response to anti-PD-1 immunotherapy.
“For example, SUV39H1 targeting activates interferon signaling pathways in breast cancer cells, leading to tumor growth arrest and improved response to anti-PD-1 immunotherapy3.”
From Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity (2025) · cites this paper as [3]
The Results section reports that SUV39H1 targeting activated IFN signaling, inhibited mammary tumor growth in mice, and improved 4T1 tumors’ response to anti-PD-1 therapy. It reports inhibited growth, not tumor growth arrest; the SUV39H1 knockdown experiment specifically used levels that permitted tumor growth. (LLM, conf=0.86)
Experimental — accuracy not yet measuredH3K9me3-mediated silencing of repetitive sequences during DNA replication is essential.
“Our previous study demonstrated this process was essential for catalyzing H3K9me3-mediated silencing of repetitive sequences during DNA replication3.”
From Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity (2025) · cites this paper as [3]
The Results section reports that FBXO44 binds H3K9me3-modified nucleosomes at the replication fork to initiate repetitive-element silencing after DNA replication. The Discussion calls FBXO44/SUV39H1 essential for this silencing in cancer cells, but says its role is cancer-cell-specific; the unqualified claim of essentiality extends beyond what the paper establishes. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTargeting specific H3K9 methyltransferases, such as SUV39H1 and SETDB1, has been shown to enhance immunotherapy responses in various cancer models.
“Targeting specific H3K9 methyltransferases, such as SUV39H1 and SETDB1, has been shown to enhance immunotherapy responses in various cancer models.”
From Multi-omics analysis identifies glioblastoma dependency on H3K9me3 methyltransferase activity (2025) · cites this paper as [3]
The Results section (page unavailable) reports that SUV39H1 knockdown and pharmacological inhibition increased 4T1 mammary tumors’ sensitivity to anti-PD-1 therapy and improved mouse survival. The cited paper does not show that targeting SETDB1 enhances immunotherapy response, and its reported treatment-response experiments do not establish the claim across various cancer models. (LLM, conf=0.88)
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Self-citationOptions for the development of colorectal cancer immunotherapy
Mustafin, R. N. (2023) · Kazan medical journal · doi:10.17816/kmj120105
Prospects of epigenetic therapy of head and neck squamous cell carcinoma
Mustafin, R. N. (2023) · Head and neck tumors (HNT) · doi:10.17650/2222-1468-2023-13-2-26-34
- Authors
- Shen, J. Z., Qiu, Z., Wu, Q., Finlay, D., Garcia, G., Sun, D., Rantala, J., Barshop, W., Hope, J. L., Gimple, R. C., Sangfelt, O., Bradley, L. M., Wohlschlegel, J., Rich, J. N., & Spruck, C.
- Affiliations
- Sanford Burnham Prebys Medical Discovery Institute (US)
- University of California San Diego (US)
- University of Sheffield (GB)
- University of California, Los Angeles (US)
- Karolinska Institutet (SE)
- Corresponding author
- Rich, Jeremy N.
- Spruck, Charles
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 184
- Issue
- 2
- Pages
- 352-369.e23
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC8043252
- OpenAlex
- W3117240765
- Cited by
- 113
- References
- 72
- Citations by year
- 2026: 14 · 2025: 23 · 2024: 25 · 2023: 23 · 2022: 19 · 2021: 7 · 2020: 2
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- California Breast Cancer Research Program
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
- Keywords
- SUV39H1, repetitive elements, replication stress, H3K9me3, interferon signaling, cancer immunotherapy response, tumor immunogenicity, cytotoxic T cell infiltration, viral mimicry, RNAi screen
- MeSH terms
- Immune Checkpoint Inhibitors, Adult, Cell Survival, DNA Replication, Female, Histones, Humans, Immunity, Interferons, Lysine, Male, Methylation, Middle Aged, Neoplasm Proteins, Neoplasms, Nucleosomes, Repetitive Sequences, Nucleic Acid, Transcription, Genetic, Signal Transduction, Gene Expression Regulation, Neoplastic, Treatment Outcome, Drug Resistance, Neoplasm, F-Box Proteins, Cell Line, Tumor, Cell Proliferation, DNA Breaks, Double-Stranded
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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