AI Article Synopsis
- The FXR1 gene is amplified in ovarian cancer patients, leading to increased levels of FXR1 mRNA and protein, which correlate with cancer cell survival and growth.
- FXR1 enhances overall protein translation in cancer cells by binding to cMYC's AU-rich elements, stabilizing its expression.
- FXR1 interacts with translation initiation factors, facilitating the circularization of cMYC mRNA and promoting its translation, thereby increasing cMYC levels in cancer cells.
Article Abstract
Fragile X-related protein-1 (FXR1) gene is highly amplified in patients with ovarian cancer, and this amplification is associated with increased expression of both FXR1 mRNA and protein. FXR1 expression directly associates with the survival and proliferation of cancer cells. Surface sensing of translation (SUnSET) assay demonstrates that FXR1 enhances the overall translation in cancer cells. Reverse-phase protein array (RPPA) reveals that cMYC is the key target of FXR1. Mechanistically, FXR1 binds to the AU-rich elements (ARE) present within the 3' untranslated region (3'UTR) of cMYC and stabilizes its expression. In addition, the RGG domain in FXR1 interacts with eIF4A1 and eIF4E proteins. These two interactions of FXR1 result in the circularization of cMYC mRNA and facilitate the recruitment of eukaryotic translation initiation factors to the translation start site. In brief, we uncover a mechanism by which FXR1 promotes cMYC levels in cancer cells.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8675433 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2021.109934 | DOI Listing |
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