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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Biomed+Sci
2018 ; 25
(1
): 57
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Incomplete cellular reprogramming of colorectal cancer cells elicits an
epithelial/mesenchymal hybrid phenotype
#MMPMID30025541
Hiew MSY
; Cheng HP
; Huang CJ
; Chong KY
; Cheong SK
; Choo KB
; Kamarul T
J Biomed Sci
2018[Jul]; 25
(1
): 57
PMID30025541
show ga
BACKGROUND: Induced pluripotency in cancer cells by ectopic expression of
pluripotency-regulating factors may be used for disease modeling of cancers.
MicroRNAs (miRNAs) are negative regulators of gene expression that play important
role in reprogramming somatic cells. However, studies on the miRNA expression
profile and the expression patterns of the mesenchymal-epithelial transition
(MET)/epithelial-mesenchymal transition (EMT) genes in induced pluripotent cancer
(iPC) cells are lacking. METHODS: iPC clones were generated from two colorectal
cancer (CRC) cell lines by retroviral transduction of the Yamanaka factors. The
iPC clones obtained were characterized by morphology, expression of pluripotency
markers and the ability to undergo in vitro tri-lineage differentiation.
Genome-wide miRNA profiles of the iPC cells were obtained by microarray analysis
and bioinformatics interrogation. Gene expression was done by real-time RT-PCR
and immuno-staining; MET/EMT protein levels were determined by western blot
analysis. RESULTS: The CRC-iPC cells showed embryonic stem cell-like features and
tri-lineage differentiation abilities. The spontaneously-differentiated post-iPC
cells obtained were highly similar to the parental CRC cells. However,
down-regulated pluripotency gene expression and failure to form teratoma
indicated that the CRC-iPC cells had only attained partial pluripotency. The
CRC-iPC cells shared similarities in the genome-wide miRNA expression profiles of
both cancer and pluripotent embryonic stem cells. One hundred and two
differentially-expressed miRNAs were identified in the CRC-iPC cells, which were
predicted by bioinformatics analysis be closely involved in regulating cellular
pluripotency and the expression of the MET/EMT genes, possibly via the
phosphatidylinositol-3 kinases-protein kinase B (PI3K-Akt) and transforming
growth factor beta (TGF-?) signaling pathways. Irregular and inconsistent
expression patterns of the EMT vimentin and Snai1 and MET E-cadherin and occludin
proteins were observed in the four CRC-iPC clones analyzed, which suggested an
epithelial/mesenchymal hybrid phenotype in the partially reprogrammed CRC cells.
MET/EMT gene expression was also generally reversed on re-differentiation, also
suggesting epigenetic regulation. CONCLUSIONS: Our data support the elite model
for cancer cell-reprogramming in which only a selected subset of cancer may be
fully reprogrammed; partial cancer cell reprogramming may also elicit an
epithelial-mesenchymal mixed phenotype, and highlight opportunities and
challenges in cancer cell-reprogramming.
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