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Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis
Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis
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Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis
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Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis
Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis

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Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis
Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis
Journal Article

Circ₀089761 accelerates colorectal cancer metastasis and immune escape via miR‐27b‐3p/PD‐L1 axis

2024
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Overview
Circular RNAs have been implicated as critical regulators in the initiation and progression of colorectal cancer (CRC). This study was intended to elucidate the functional significance of the circ₀089761/miR‐27b‐3p/programmed cell death ligand 1 (PD‐L1) axis in CRC. Our findings indicated that circ₀089761 expression was significantly elevated in CRC tissues and cell lines. Furthermore, the high expression of circ₀089761 was correlated with TNM stage and tumor size. Silencing circ₀089761 inhibited CRC cell proliferation, migration, and invasion, and increased apoptosis. Mechanistically, circ₀089761 facilitated its biological function by binding to miR‐27b‐3p to upregulate PD‐L1 expression in CRC. Coculture experiments confirmed that low expression of circ₀089761 impeded CD8 + T cell apoptosis and depletion, activated CD8 + T cell function, and increased secretion of the immune effector cytokines IFN‐γ, TNF‐α, perforin, and granzyme‐B. MiR‐27b‐3p inhibition or PD‐L1 overexpression partially impeded CD8 + T cell function. The circ₀089761/miR‐27b‐3p/PD‐L1 axis is postulated to exert pivotal functions in the mechanistic progression of CRC. Furthermore, it holds promising prospects as a feasible biomarker and therapeutic target for CRC.
Publisher
John Wiley and Sons Inc,Wiley