Renal angiomyolipomas (AMLs) are benign kidney tumors that can exhibit aggressive behavior. Previous studies have suggested the involvement of the ERK/MAPK pathway in tumor growth, but the role of makorin ring finger protein 1 (MKRN1), an E3 ubiquitin ligase, in AML pathogenesis remains unclear. This study explores the role of MKRN1 in regulating cell proliferation in AMLs by modulating the ERK/MAPK pathway.

MKRN1 expression was assessed in AML tissues via immunohistochemistry (IHC) and quantitative real-time PCR. AML cell lines (SV7, UMB) were transfected with MKRN1 expression plasmids. Cell proliferation was analyzed using the Cell Counting Kit-8 (CCK-8) assay. Gene set enrichment analysis (GSEA) of RNA-Seq data and Western blotting were conducted to investigate the role of MKRN1 in the ERK/MAPK pathway.

MKRN1 expression was significantly lower in AML tissues compared to adjacent normal renal tissues. Overexpression of MKRN1 inhibited AML cell proliferation. GSEA revealed that MKRN1 downregulates the ERK/MAPK pathway, which was confirmed by a significant reduction in phosphorylated ERK (p-ERK) levels in MKRN1-overexpressing cells.

MKRN1 acts as a tumor suppressor in renal AMLs by downregulating the ERK/MAPK signaling pathway, leading to reduced cell proliferation. These findings suggest that MKRN1 could serve as a potential biomarker and therapeutic target for AML management.