Abstract
The phosphatase of regenerating liver (PRL) family of phosphatases, consisting of PRL-1, PRL-2, and PRL-3, represents an intriguing group of proteins being validated as biomarkers and therapeutic targets in cancer. Individual PRLs are overexpressed in a variety of cancer cell lines and tissues when compared with their normal counterparts. More importantly, several recent studies have shown that PRL-3 is expressed at higher levels and at a greater frequency in colorectal cancer metastases compared with primary colorectal tumors and normal colon tissue. Ectopic expression of PRLs in nontumorigenic cells can influence proliferation and the migratory and invasive properties of cells, while knockdown of endogenous PRL-3 or PRL-1 in cancerous cells using small interfering RNA can abrogate cell motility and ability to metastasize in a mouse model. However, the exact biological function and cellular substrates of the PRLs remain unclear. This review will discuss what is known about the PRLs, what makes the PRLs possible attractive targets for therapeutic intervention, and the possible future directions in PRL biology and inhibitor identification.
Highlights
Phosphorylation and dephosphorylation are major regulatory events affecting the functional activities of diverse proteins that modulate cellular processes, such as transcriptional regulation, apoptosis, cell cycle progression, protein degradation, and protein trafficking [1, 2]
Bardelli et al [22] observed high phosphatase of regenerating liver (PRL)-3 mRNA expression in metastatic lesions derived from colorectal cancers regardless of the site of metastasis, whereas low levels of PRL-3 were observed in non – colorectal cancer metastases to the lung or the liver. These results indicated that PRL-3 might be involved in cell type – specific metastatic processes
The PRL family of phosphatases represents a group of enzymes for further validation as metastasis biomarkers and as possible therapeutic targets
Summary
Phosphorylation and dephosphorylation are major regulatory events affecting the functional activities of diverse proteins that modulate cellular processes, such as transcriptional regulation, apoptosis, cell cycle progression, protein degradation, and protein trafficking [1, 2]. Bardelli et al [22] observed high PRL-3 mRNA expression in metastatic lesions derived from colorectal cancers regardless of the site of metastasis (liver, lung, brain, or ovary), whereas low levels of PRL-3 were observed in non – colorectal cancer metastases to the lung (pancreas and stomach cancers) or the liver (pancreas, esophagus, and stomach cancers). These results indicated that PRL-3 might be involved in cell type – specific metastatic processes. Overexpression of PRL-1 or PRL-2 in D27 hamster pancreatic ductal epithelial cells resulted in loss of contact
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
