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Genomic studies controvert the existence of the CUX1 p75 isoform. | LitMetric

AI Article Synopsis

  • - CUX1, a gene that acts as a transcription factor, is often deleted or mutated in various tumors, particularly in myeloid neoplasms where it leads to a poor prognosis.
  • - While some studies suggest CUX1 has oncogenic roles through shorter isoforms (p75 and p110) in solid tumors, our research confirms that hematopoietic cells predominantly express the full-length p200 isoform instead.
  • - Our extensive analysis, involving several scientific methods, found no evidence for the p75 isoform, suggesting that earlier studies attributing oncogenic functions to this variant need to be reevaluated.

Article Abstract

CUX1, encoding a homeodomain-containing transcription factor, is recurrently deleted or mutated in multiple tumor types. In myeloid neoplasms, CUX1 deletion or mutation carries a poor prognosis. We have previously established that CUX1 functions as a tumor suppressor in hematopoietic cells across multiple organisms. Others, however, have described oncogenic functions of CUX1 in solid tumors, often attributed to truncated CUX1 isoforms, p75 and p110, generated by an alternative transcriptional start site or post-translational cleavage, respectively. Given the clinical relevance, it is imperative to clarify these discrepant activities. Herein, we sought to determine the CUX1 isoforms expressed in hematopoietic cells and find that they express the full-length p200 isoform. Through the course of this analysis, we found no evidence of the p75 alternative transcript in any cell type examined. Using an array of orthogonal approaches, including biochemistry, proteomics, CRISPR/Cas9 genomic editing, and analysis of functional genomics datasets across a spectrum of normal and malignant tissue types, we found no data to support the existence of the CUX1 p75 isoform as previously described. Based on these results, prior studies of p75 require reevaluation, including the interpretation of oncogenic roles attributed to CUX1.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8741762PMC
http://dx.doi.org/10.1038/s41598-021-03930-4DOI Listing

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