AI Article Synopsis

  • * The upregulation of IQGAP3 in cancer is linked to the re-expression of IGF2BP1, which stabilizes its transcripts and promotes its growth-stimulating effects.
  • * Understanding how IQGAP3 expression is regulated could lead to new drug targets to prevent cancer growth driven by aberrant stem cell proliferation.

Article Abstract

We reported earlier that IQGAP3 is an important stem cell factor in rapidly proliferating isthmus stem cells in the stomach and that IQGAP3 expression is robustly induced in terminally differentiated chief cells and de-differentiated cells following tissue damage. The elevated IQGAP3 expression in cancer and its association with metastasis suggest a fundamental role for IQGAP3 in proliferating cancer stem cells. What causes IQGAP3 upregulation in cancer is unclear. Here, we show that IGF2BP1 and IQGAP3 expression levels are highest in the blastocyst, with both decreasing during adulthood. This suggests that IQGAP3, like IGF2BP1, is an early developmental gene that is aberrantly upregulated upon re-expression of IGF2BP1 during carcinogenesis. IGF2BP1 binds and stabilizes mA-modified IQGAP3 transcripts. Downstream targets of IGF2BP1, namely SRF and FOXM1, also upregulate IQGAP3 expression. These multiple layers of IQGAP3 regulation, which may safeguard against inappropriate stem cell proliferation, present additional drug targets to inhibit IQGAP3-driven malignant growth.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9547305PMC
http://dx.doi.org/10.1016/j.isci.2022.105194DOI Listing

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