The Role of Myoferlin in Vesicle Trafficking and the Effects of Its Overexpression in Prostate Cancer

Myoferlin (MYOF), a member of the ferlin protein family, is a type II transmembrane protein with a single transmembrane domain at its carboxyl terminus. It plays critical roles in membrane vesicle trafficking, fusion, repair, and endocytosis, and is overexpressed in several cancers, which may contribute to malignant transformation. In this study, we demonstrated that MYOF is overexpressed in human prostate cancer cells, and knockdown of MYOF significantly reduced migration and invasion abilities. We also found that higher levels of MYOF expression were associated with shorter PSA recurrence-free survival times in patients who underwent radical prostatectomy. To our knowledge, this is the first study to demonstrate the clinical significance of MYOF expression in prostate cancer and to identify DNAJC13 as a novel MYOF-interacting protein. These findings suggest that MYOF impacts the malignancy and prognosis of prostate cancer. Additionally, we identified that MYOF interacts with DnaJ heat shock protein family member C13 (DNAJC13), an endosome-associated protein. Immunocytochemistry revealed that MYOF co-localized with DNAJC13 and lysosomes. The newly identified interaction partners of MYOF suggest its involvement in promoting cancer invasion through endosomal and lysosomal pathways. Although functional validation of this interaction remains to be elucidated, our results provide important insights for future mechanistic studies. These findings provide insights into the functional role of MYOF in cancer invasion and metastasis, suggesting that MYOF could be a novel therapeutic target for metastatic prostate cancer.