ELF3 regulates epithelial-mesenchymal transition through TPM1 and promotes the development of endometrial cancer.

Endometrial cancer (EC) is one of the common malignancies of the female reproductive system, and metastasis is critical to the progression and prognosis of EC. As a transcription factor, ELF3 is widely involved in the regulation of cancer cell growth and metastasis, but its role in EC is unclear. The purpose of this study was to explore the role and mechanism of ELF3 in regulating EC progression. In this study, we collected 8 pairs of EC tissue and normal paracancerous endometrial tissue, and injected human endometrial cancer cells (Ishikawa) into the left axilla of nude mice to construct a model of subcutaneous tumorigenesis in nude mice. The growth of Ishikawa cells and tumor tissues of EC nude mice was evaluated by CCK-8, clone formation assay, immunohistochemistry, etc., and the expression of related proteins and genes was detected by Western blot and RT-qPCR. In this study, it was found that the expression of ELF3 was up-regulated in EC, and knockdown of ELF3 could inhibit the proliferative activity and colony formation of EC cells, promote the expression of E-cadherin, inhibit the expression of N-cadherin and Vimentin, and reduce the epithelial-mesenchymal transition (EMT) of EC cells, thereby inhibiting the migration of EC cells to a certain extent and alleviating the development of EC in vivo. Mechanistically, ELF3 inhibits TPM1 transcription by binding to the promoter region of TPM1 gene, thereby inhibiting TPM1 expression, promoting EMT, proliferation and migration of EC cells, and accelerating the occurrence and development of EC in vivo. ELF3 promotes the development of EC through TPM1 regulation of EMT, and inhibition of ELF3 may become a potential new target for the treatment of EC.