Abstract
IntroductionProstate cancer (PC) is the second greatest cause of cancer deaths globally. PC presents a poor prognosis once it metastasizes. There is considerable proof of vital epithelial–mesenchymal transition (EMT) functionality in PC metastasis. Previous studies revealed that melanophilin (MLPH) is associated with PC; however, its role in PC remains poorly understood.MethodsBioinformatics analyses were performed. The cellular responses to MLPH knockdown were examined in HCC cell lines via wound healing assay, migration and invasion assay, Western blotting.ResultsAnalysis of the PROGgeneV2 database revealed that high MLPH expression might indicate poor overall survival. MLPH knockdown reduced PC cell migration, proliferation, and invasion. MLPH downregulation in vivo resulted in a lower growth rate and fewer metastatic nodules in lung tissues. Furthermore, MLPH knockdown recovered downregulated expression of the mesenchymal marker N-cadherin and the epithelial marker E-cadherin following a decrease in β-catenin.ConclusionThese results indicate that progression of PC is stimulated via MLPH-dependent initiation of the EMT.
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