circEIF3I Promotes Colorectal Cancer Metastasis by Regulating the miR‐328‐3p/NCAPH Axis

ABSTRACT Colorectal cancer (CRC) is the most common gastrointestinal malignancy, with its recurrence and metastasis significantly affecting patient survival. Circular RNAs (circRNAs), a novel class of noncoding RNAs, have emerged as crucial contributors to CRC pathogenesis. However, the role of circEIF3I in CRC metastasis remains unclear. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was applied to assess circEIF3I, microRNA (miR)‐328‐3p, and NCAPH expression. CRC cell migration and invasion were determined via Transwell assays. Western blot analysis was utilized to define the protein expression of epithelial‐mesenchymal transition (EMT) markers and NCAPH. Xenograft tumor was established for exploration into the function of circEIF3I in CRC metastasis to the liver and lung. The binding between miR‐328‐3p and circEIF3I or NCAPH was predicted through ENCORI or TargetScan platform and ascertained through dual‐luciferase reporter assays. circEIF3I and NCAPH expression were found to be elevated in CRC tissues and cells, while miR‐328‐3p was downregulated. Functionally, circEIF3I knockdown inhibited CRC cell migration, invasion, EMT, and tumor metastasis. Mechanistic analyses revealed that circEIF3I can target miR‐328‐3p, while NCAPH was targeted by miR‐328‐3p. Furthermore, circEIF3I facilitated NCAPH expression in CRC cells by sequestering miR‐328‐3p. Notably, miR‐328‐3p inhibitor or NCAPH overexpression negated the effects of circEIF3I knockdown on preventing CRC progression in vitro. Taken together, circEIF3I elevated NCAPH expression by sponging miR‐328‐3p, thereby promoting CRC metastasis. These findings suggest that the circEIF3I/miR‐328‐3p/NCAPH axis represents a novel therapeutic target for CRC.