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| Home > Publications database > Enhanced IGFL1 translation in response to IL-1β is controlled by distinct 3'UTR elements. |
| Home > Publications database > Enhanced IGFL1 translation in response to IL-1β is controlled by distinct 3'UTR elements. |
| Journal Article | DKFZ-2026-01558 |
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2026
PLOS
San Francisco, California, US
Abstract: Translation is a crucial regulatory mechanism involved in several diseases, including cancer, where pro-inflammatory conditions within the microenvironment have been shown to modulate the translation of specific mRNAs. In the present study, we focused on the regulation of insulin growth factor-like family member 1 (IGFL1) in MCF7 breast cancer cells in response to pro-inflammatory IL-1β and observed an induction of both transcription and translation. We characterized the 3' untranslated region as regulatory hub for the post-transcriptional regulation and identified a distinct G-rich region to confer the IL-1β-dependent translational increase. Our study therefore provides new insights into the translation regulation of IGFL1 in the context of an inflammatory tumor microenvironment.
Keyword(s): Humans (MeSH) ; Interleukin-1beta: pharmacology (MeSH) ; 3' Untranslated Regions: genetics (MeSH) ; Protein Biosynthesis: drug effects (MeSH) ; Insulin-Like Peptides: genetics (MeSH) ; Insulin-Like Peptides: metabolism (MeSH) ; MCF-7 Cells (MeSH) ; RNA, Messenger: genetics (MeSH) ; RNA, Messenger: metabolism (MeSH) ; Gene Expression Regulation, Neoplastic: drug effects (MeSH) ; Interleukin-1beta ; 3' Untranslated Regions ; Insulin-Like Peptides ; RNA, Messenger
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