MicroRNA-148a-3p Regulates Colorectal Cancer Cell Proliferation and Immune Escape through KLF4

MicroRNA (miR)-148a-3p is most frequently upregulated in solid tumors, such as colorectalcancer (CRC). This study aimed to elucidate the role of miR-148a-3p in CRC cell proliferation andimmune escape and its potential mechanism.miR-148a-3p and Kruppel-like transcription factor 4 (KLF4) expressions were quantified bywestern blot and quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation,migration, invasion, epithelial-mesenchymal transition (EMT), and immune evasion abilities of CRCcells were evaluated with the cell counting kit-8 assay, Transwell, western blot, and enzyme-linkedimmunosorbent assays. The proliferation or apoptosis of CD8+ and CD4+ T cells after coculturewith CRC cells was assessed by flow cytometry. Dual-luciferase reporter gene testing was used tovalidate the targeting association between KLF4 and miR-148a-3p. A nude mouse subcutaneousgraft tumor model was constructed, and CD8+ T cell infiltration was detected byimmunohistochemistry and flow cytometry.miR-148a-3p exhibited a high level, while KLF4 was under-expressed in CRC cells; miR-148a-3p negatively regulated the KLF4 level. Overexpression of miR-148a-3p enhanced CRC cellproliferation, migration, invasion, EMT, and immune escape; silencing miR-148a-3p caused theopposite trend; moreover, the said biological functions of CRC cells were weakened withoverexpression of KLF4 but enhanced with silencing of KLF4; silencing KLF4 weakened theinfluences of dampened miR-148a-3p on CRC development. Silencing miR-148a-3p promoted theinfiltration of CD8+ T cells and inhibited tumor growth.In summary, miR-148a-3p promotes CRC cell proliferation and immune evasion by regulatingthe expression of KLF4. This finding can be used for reference when developing a new way of CRCtreatment.