Myelin and lymphocyte protein 2 regulates cell proliferation and metastasis through the Notch pathway in prostate adenocarcinoma.

Abstract

BackgroundMyelin and lymphocyte protein 2 (MAL2) is a proven oncogene in some human tumors. However, currently, little is known about the function of MAL2 in prostate adenocarcinoma (PRAD). This study sought to investigate the role of MAL2 on PRAD progression.MethodsMAL2 expression in PRAD was first analyzed by the Gene Expression Profiling Interactive Analysis (GEPIA) database. The reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay and Western blot assay were used to detect the expression of MAL2 in PRAD tissues and cell lines. Additionally, immunohistochemistry (IHC) straining was used to detect the expression of MAL2 in PRAD pathological tissues. The Cell Counting Kit-8 (CCK-8) assay, clone formation assay and Flow cytometry were performed to investigate the effect of MAL2 on PRAD cell proliferation and cell apoptosis. Cell migration and invasion were measured by Transwell assay. The effect of MAL2 on epithelial-mesenchymal transition (EMT) progression and the Notch signaling pathway in PRAD was also investigated.ResultsMAL2 was discovered to be obviously upregulated in PRAD tissues and cell lines. The upregulation of MAL2 was closely associated with tumor, nodes and metastases (TNM) stage, the Gleason score and metastasis of PRAD patients, and affected the prognosis of PRAD patients. Functionally, the depletion of MAL2 suppressed cell proliferation, migration, invasion, and EMT progression, and promoted cell apoptosis of PRAD cells. In an in vivo experiment, MAL2 knockdown significantly suppressed tumor growth in mice. Further, inhibiting the Notch pathway reversed the effect of MAL2 knockdown on PRAD progression.ConclusionsIn sum, MAL2 was found to be upregulated in PRAD, and appears to act as a carcinogen in PRAD. Additionally, MAL2 appears to regulate PRAD progression through the Notch signaling pathway.