E2F7/Beclin-1 Pathway: Influencing Autophagy and EMT in ccRCC.

Abstract

Purpose: The deficiency of the current study of ccRCC lies in the incomplete understanding of the interaction between the E2F7/Beclin-1 pathway, autophagy, and EMT. This study aims to investigate the influence of the E2F7/Beclin-1 pathway on autophagy and EMT in human ccRCC.

Methods: An entire collection of 24 samples, including ccRCC tissues and their corresponding adjacent tissues, were selected for this study. Immunohistochemistry was implemented to analyze the expression and distribution of E2F7 in ccRCC tissues and adjacent tissues. Western blot techniques and RT-qPCR were used to measure the amounts of E2F7 protein and mRNA expression in ccRCC alongside adjacent tissues, as well as autophagy-related molecule Beclin-1, LC3, and EMT-related molecule E-cadherin. Analysis was done on the relationship between clinical pathologic characteristics and E2F7 expression. In vitro mechanistic validation was conducted using the ccRCC cell line (786-0 cells) transfected with E2F7 overexpression plasmid and E2F7-specific inhibitor si-E2F7.

Results: Comparing ccRCC tissues to surrounding tissues, Beclin-1, LC3, and E-cadherin expression levels decreased considerably. Conversely, ccRCC tissues exhibited considerably higher expression levels of E2F7. Silencing E2F7 increased protein and mRNA expression levels of Beclin-1, LC3, and E-cadherin.

Conclusion: In renal cancer tissues, a robust inverse correlation was detected between the expression of E2F7 and that of Beclin-1, LC3, and E-cadherin. E2F7 expression showed a substantial beneficial association. Notably, elevated E2F7 expression was associated with advanced clinical and pathologic stages of the tumor. A dual-luciferase assay confirmed the interaction between E2F7 and Beclin-1.