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| Status |
Public on May 01, 2024 |
| Title |
IRF3 drives replication stress signaling and determines sensitivity to genotoxic agents in triple-negative breast cancer cells |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Interferon-β signaling has been shown to play important roles in anti-virus as well as anti-tumor immunity. We here report that the key transcription factor in type I interferon signaling, IRF3, as well as downstream interferon-β are able to induce replication stress signaling in triple-negative breast cancer cells. IRF3 overexpression sensitizes triple-negative breast cancer cells to several genotoxic agents. Addition of IFN-β, a key downstream cytokine of IRF3,reduced replication fork speed and activated ATR-CHK1 signaling. Conversely, type I interferon-neutralizing antibodies or nucleosides supplementation rescued IRF3-induced replication stress.
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| Overall design |
We treated two triple-negative breast cancer cell lines, HCC38 and MDA-MB-231, with interferon-β (400 IU/mL) for 48 hours. We then performed gene expression profiling analysis using data obtained from RNA-seq of untreated samples and interferon-β-treated samples.
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| Contributor(s) |
van Vugt MA, Chen M |
| Citation missing |
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| Submission date |
Apr 15, 2024 |
| Last update date |
May 01, 2024 |
| Contact name |
Marcel van Vugt |
| Organization name |
University Medical Center Groningen
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| Street address |
Hanzeplein 1
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| City |
Groningen |
| State/province |
Netherlands |
| ZIP/Postal code |
9713 GZ |
| Country |
Netherlands |
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| Platforms (1) |
| GPL24676 |
Illumina NovaSeq 6000 (Homo sapiens) |
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| Samples (12)
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| Relations |
| BioProject |
PRJNA1100437 |
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