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bioRxiv · 10.64898/2026.01.21.700974

Enhanced IGFL1 translation in response to IL-1β is controlled by distinct 3UTR elements

Cardamone, G.·Flohr, M.·Raue, R.·Bode, I.·Meyer, S. P.·Hauns, S.·Backofen, R.·Schmid, T.
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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-1{beta} 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-1{beta}-dependent translational increase. Our study therefore provides new insights into the translation regulation of IGFL1 in the context of an inflammatory tumor microenvironment.

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Cardamone, G., Flohr, M., Raue, R., Bode, I., Meyer, S. P., Hauns, S., Backofen, R., Schmid, T.. 2026-01-22. Enhanced IGFL1 translation in response to IL-1β is controlled by distinct 3UTR elements. https://doi.org/10.64898/2026.01.21.700974

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