Abstract
Akin to many other cancers, metastasis is the predominant cause of lethality in prostate cancer (PCa). Research in the past decade or so has revealed that although metastatic manifestation is a multi-step and complex process that is orchestrated by distinct cellular and molecular mechanisms, the process in itself is an extremely inefficient one. It is now becoming increasingly evident that PCa cells employ a plethora of strategies to make the most of this inefficient process. These strategies include priming the metastatic sites ahead of colonization, devising ways to metastasize to specific organs, outsmarting the host defense surveillance, lying in a dormant state at the metastatic site for prolonged periods, and widespread reprogramming of the gene expression to suit their needs. Based on established, recent, and evolving lines of research, this review is an attempt to understand PCa metastasis from the perspective of military combat, wherein strategic maneuvering instead of brute force often plays a decisive role in the outcome.
Highlights
Similar to many other cancers, metastasis is the predominant cause of morbidity and mortality in advanced prostate cancer (PCa)
This isunderscored by the fact that eight of the 12 cancers followed for a decade (2005–2015) showed a decrease in the 5-year survival rates of patients diagnosed with metastatic disease, and PCa was among these cancers [1]
Studies have reported that metastatic castrate resistant PCa (CRPC) specimens are linked with a higher number of genomic sites showing open chromatin conformation as compared with primary untreated PCa or locally recurrent PCa specimens [132,134]. This suggests extensive chromatin reprogramming during the progression to castrate resistant disease, and inter-patient sample analysis has revealed that the core set of open chromatin regions in the genome, while similar in benign prostatic hyperplasia (BPH) and primary PCa, were varied in CRPC samples [132]
Summary
Similar to many other cancers, metastasis is the predominant cause of morbidity and mortality in advanced prostate cancer (PCa). In addition to the primary tumor microenvironment, there is growing evidence that EVs can be released in several body fluids, as has been reported in PCa [33], and EVs are thought to play a role in the metastatic spread of PCa. In line with this hypothesis, miRNAs from EVs have been shown to correlate with PCa metastasis and several reports have suggested that these miRNAs could be utilized as potential biomarkers and therapeutic targets for PCa [34].
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