Microfibril-associated protein 2 interacts with LEF1/TCF7 and immune infiltration in uterine corpus endometrial carcinoma.

INTRODUCTION: The present study aimed to investigate the involvement of microfibril-associated protein 2 (MFAP2), a multifunctional secreted protein and constituent of extracellular matrix microfibrils, in the tumorigenicity of uterine corpus endometrial carcinoma (UCEC). MATERIAL AND METHODS: The mRNA expression levels of MFAP2A were detected in a total of 52 pairs of UCEC and adjacent non-tumorous tissues. Cell proliferation, migration and invasion, as well as cell apoptosis, were assessed using CCK8, Transwell and TUNEL assays, respectively. In addition, overall survival, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment and gene alterations were determined by bioinformatic analysis. RESULTS: The results showed that MFAP2 and transcription factor 7 like 1 (TCF7L1) were significantly upregulated in UCEC tissues compared with normal non-tumoral tissues. Also, a notable positive association between MFAP2 and TCF7L1 was observed in UCEC tissues. Furthermore, MFAP2 silencing notably attenuated the proliferation, migration, and invasion, and enhanced the apoptosis of UCEC cells. However, overexpression of MFAP2 abrogated the anti-tumor effect of TCF7L1 silencing on UCEC cell lines. Our study also revealed a negative correlation between MFAP2 and Immunoscore. CONCLUSIONS: The present study suggested that MFAP2 could be involved in the carcinogenic progression of UCEC via the β-catenin/TCF7L1 axis. MFAP2 overexpression may contribute to immunosuppression in UCEC patients.