CSE1L, DIDO1 and RBM39 in colorectal adenoma to carcinoma progression

Cell Oncol (Dordr). 2012 Aug;35(4):293-300. doi: 10.1007/s13402-012-0088-2. Epub 2012 Jun 19.


Background: Gain of chromosome 20q is an important factor in the progression from colorectal adenomas to carcinomas. Genes that drive 20q gain are expected to show correlation of mRNA and protein expression levels with 20q DNA copy number status while functionally influencing cancer processes. CSE1L, DIDO1 and RBM39 are located on the 20q amplicon and affect processes such as cell viability and anchorage-independent growth in colorectal cancer. This study aimed to investigate whether CSE1L, DIDO1 and RBM39 may drive 20q amplification.

Methods: Protein expression levels were examined by immunohistochemical evaluation of tissue microarrays containing a series of colorectal adenoma and carcinoma samples, which were characterized by genome-wide (microarray-based) DNA and mRNA profiling.

Results: CSE1L, DIDO1 and RBM39 mRNA expression levels correlated with chromosome 20q DNA copy number status. CSE1L protein expression was not associated with 20q gain, although its expression was increased in carcinomas compared to adenomas. DIDO1 and RBM39 protein expression was quite strong in the majority of tumors irrespective of 20q DNA copy number status.

Conclusion: The lack of correlation between protein expression levels and 20q DNA copy number status implies that CSE1L, DIDO1 and RBM39 are merely passengers rather than drivers of chromosome 20q gain in colorectal adenoma-to-carcinoma progression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoma / genetics*
  • Adenoma / metabolism
  • Adenoma / pathology
  • Carcinoma / genetics*
  • Carcinoma / metabolism
  • Carcinoma / pathology
  • Cellular Apoptosis Susceptibility Protein / genetics*
  • Cellular Apoptosis Susceptibility Protein / metabolism
  • Chromosome Aberrations
  • Chromosomes, Human, Pair 20 / genetics
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / metabolism
  • Colorectal Neoplasms / pathology
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Disease Progression
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Immunohistochemistry
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • RNA-Binding Proteins / genetics*
  • RNA-Binding Proteins / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tissue Array Analysis


  • Cellular Apoptosis Susceptibility Protein
  • DIDO1 protein, human
  • DNA-Binding Proteins
  • HCC1 autoantigen
  • Nuclear Proteins
  • RNA, Messenger
  • RNA-Binding Proteins