Search

This document is a retraction notice from the journal OncoTargets & Therapy regarding an article titled "MLPH Accelerates the Epithelial–Mesenchymal Transition in Prostate Cancer." The retraction is due to concerns about the duplication of images from Figure 3 with images from other unrelated articles. The authors did not respond to queries or provide an explanation for the duplicated images. The retracted article will remain online but will be digitally watermarked as "Retracted." [Extracted from the article]

Introduction: 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. Methods: 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. Results: 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. Conclusion: These results indicate that progression of PC is stimulated via MLPH-dependent initiation of the EMT. [ABSTRACT FROM AUTHOR]