Hsa_circ_0000423 promotes colorectal cancer EMT and immune escape by competitive adsorption of miR-369-3p mediating CCND1 expression

Hsa_circ_0000423通过竞争性吸附miR-369-3p介导CCND1表达促进结直肠癌EMT和免疫逃逸

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作者:TianFu Huang, KaiHai Jiang, LinTao Li, GuangSheng Li, YuSheng Cao, XuSen Huang

Background

This investigation evaluated the mechanism of hsa_circ_0000423 in colorectal cancer (CRC).

Conclusion

Hsa_circ_0000423 promotes CCND1 expression through competitive binding of miR-369-3p and promotes CRC cell development and immune escape.

Methods

The hsa_circ_0000423 gene was identified by bioinformatics analyses of GEO circRNA microarrays, and its expression in CRC was investigated. Based on this, in vitro experiments were conducted. Assays with dual luciferase reporter and RIP were conducted to detect interactions between hsa_circ_0000423, miR-369-3p and CCND1. Cell proliferation was measured by MTT and colony formation assay assays, apoptosis was detected by flow cytometry, migration and invasion were detected by Transwell, and expression of EMT-related proteins was detected by Western Blot. SW480 cells and T cells were co-cultured to assess immune escape.

Results

hsa_circ_0000423 and CCND1 were elevated in CRC while miR-369-3p was downregulated Silencing hsa_circ_0000423 resulted in reduced CCND1 expression by upregulating miR-369-3p. Overexpressing CCND1 or down-regulating miR-369-3p both interrupted the anti-tumor role of silencing hsa_circ_0000423 on CRC cells.

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