MLPH Accelerates the Epithelial-Mesenchymal Transition in Prostate Cancer

OncoTargets and Therapy
Tianbiao ZhangWeixing Zhang

Abstract

Prostate 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. Bioinformatics 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. Analysis 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. These results indicate that progression of PC is stimulated via MLPH-dependent initiation of the EMT.

Methods Mentioned

BETA
Reverse Transcription Polymerase
protein assay
electrophoresis
Assay
xenograft

Software Mentioned

Bio
Rad Quantity One
ImageJ

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