CSE1L, DIDO1 and RBM39 in colorectal adenoma to carcinoma progression.
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.


CONCLUSIONS
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.
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands.
Anke H
AH
Sillars-Hardebol
Beatriz
B
Carvalho
Jeroen A M
JA
Beliën
Meike
M
de Wit
Pien M
PM
Delis-van Diemen
Marianne
M
Tijssen
Mark A
MA
van de Wiel
Fredrik
F
Pontén
Gerrit A
GA
Meijer
Remond J A
RJ
Fijneman
D000236:Adenoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002277:Carcinoma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D029563:Cellular Apoptosis Susceptibility Protein / Q000235:genetics* / Q000378:metabolism; D002869:Chromosome Aberrations; D002890:Chromosomes, Human, Pair 20 / Q000235:genetics; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D018450:Disease Progression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D009687:Nuclear Proteins / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D046888:Tissue Array Analysis
D029563:Cellular Apoptosis Susceptibility Protein; C518584:DIDO1 protein, human; D004268:DNA-Binding Proteins; C084105:HCC1 autoantigen; D009687:Nuclear Proteins; D012333:RNA, Messenger; D016601:RNA-Binding Proteins