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چکیده
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A complex and gradual process, the epithelial–mesenchymal transition (EMT) occurs both
during embryonic development and tumor progression. Cells undergo a transition from
an epithelial to a mesenchymal state throughout this process. More and more evidence
points to EMT as a cause of increased metastatic spread of prostate cancer (PCa), along
with stemness enhancement and therapy resistance. Here, we used bioinformatic methods
to analyze gene expression microarray data, single-cell RNA sequencing, oncogenes,
and tumor suppressor genes (TSGs) in order to reconstruct the network of differentially
expressed genes (DEGs) involved in the epithelial–mesenchymal transition with PCa. No
prior study has documented this sort of analysis. We next validated our results using data
from the Cancer Genome Atlas (TCGA), which included microarray and single-cell RNA
sequencing. Potentially useful in PCa diagnosis and treatment are extracellular matrix
in epithelial–mesenchymal transition genes, including ITGBL1, DSC3, COL4A6, ANGPT1,
ARMCX1, MICAL2, and EPHA5. In this study, we aimed to shed light on the molecular
characteristics and pathways of DEGs in PCa, as well as to identify possible biomarkers
that are important in the development and advancement of this cancer. These insights
have important implications for understanding prostate cancer progression and for the
development of therapeutic strategies targeting ECM-mediated pathways.
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