Globally, the cancer associated deaths are generally attributed to the spread of cancerous cells or their features to
the nearby or distant secondary organs by a process known as metastasis. Among other factors, the metastatic dissemination
of cancer cells is attributed to the reactivation of an evolutionary conserved developmental program known as epithelial to
mesenchymal transition (EMT). During EMT, fully differentiated epithelial cells undergo a series of dramatic changes in
their morphology, along with loss of cell to cell contact and matrix remodeling into less differentiated and invasive mesenchymal
cells. Many studies provide evidence for the existence of EMT like states in prostate cancer (PCa) and suggest its
possible involvement in PCa progression and metastasis. At the same time, the lack of conclusive evidence regarding the
presence of full EMT in human PCa samples has somewhat dampened the interest in the field. However, ongoing EMT research
provides new perspectives and unveils the enormous potential of this field in tailoring new therapeutic regimens for PCa management.
This review summarizes the role of many transcription factors and other molecules that drive EMT during prostate tumorigenesis
Keywords: Epithelial mesenchymal transition, prostate cancer, transcription factors, endoplasmic reticulum, stress, signaling, Y Box Protein-1.
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