Conclusion
Knockdown of GGTLC1 attenuates EC development through the TGF-β/Smad pathway, positioning GGTLC1 as a promising target for EC treatment.
Methods
Bioinformatic tools and databases were used to analyze GGTLC1 and its associated gene expression in EC tissues. Functional enrichment explorations and immune infiltration analyses were conducted, together with investigation into the methylation status of GGTLC1. Western blotting and Quantitative real-time PCR quantified expression levels. Additional experimental methodologies elucidated the role of GGTLC1 in EC progression. Transcriptome sequencing identified potential regulatory pathways for GGTLC1, and tumor growth was evaluated in vivo using HEC-1A cells in nude mice.
Purpose
Endometrial cancer (EC) poses a serious risk to females worldwide; thus, a deep understanding of EC is urgently required. The role and mechanisms of gamma-glutamyltransferase light chain 1 (GGTLC1) in EC remain obscure. This study aims to elucidate the function and mechanisms underlying GGTLC1's involvement in EC.
Results
GGTLC1 was upregulated and negatively correlated with immune cell infiltration and DNA methylation in EC. Cell migration and proliferation were reduced following GGTLC1 knockdown, together with arrest at the G0/G1 phase and an upsurge in apoptosis. Compared to the knockdown group, TGF-β/Smad signaling pathway was up-regulated in the negative control group of EC cells by transcriptome analysis. The levels of TGF-β, pSmad2, and pSmad3 followed the same decreasing trend, whereas Smad3 and Smad2 protein levels remained unchanged.