Inhibitory effect on endometrial cancer: Collagen type XII α1 chain.

Abstract

Objective: Endometrial cancer (EC) is one of the most common gynecological malignancies, and it poses a considerable threat to women's lives. Therefore, searching for EC inhibitors and exploring the potential mechanism of action is particularly important. This article aims to investigate the potential effect of collagen type XII α1 chain (COL12A1) on macrophage polarization and its subsequent influence on the biological behavior of EC cells to further elucidate the underlying mechanisms of EC development.

Material and methods: Quantitative real-time polymerase chain reaction and Western blot were used to detect the expression levels of COL12A1 messenger RNA and protein in EC cells. A subcutaneous tumor formation assay was performed in nude mice to evaluate the effect of COL12A1 on EC cell growth in vivo. Flow cytometry was utilized to assess the expression levels of macrophage surface markers under different treatments. Cell counting kit-8, Transwell assay, and Western blot experiments were conducted to investigate the effects of COL12A1 knockdown and various macrophage treatments on the biological behavior of EC cells.

Results: The expression of COL12A1 was upregulated in EC cells. Knockdown of COL12A1 significantly inhibited the viability, invasion, migration, and extracellular matrix abilities of EC cells and tumor growth in vivo. Overexpression of COL12A1 significantly promoted M2-type macrophage polarization, which enhanced the invasion, migration, and epithelial-mesenchymal transition abilities of EC cells.

Conclusion: The expression of COL12A1 is upregulated in EC, and COL12A1 promotes EC cell invasion and migration by activating macrophage M2 polarization.