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 colorectal cancer (crc). this study aimed to elucidate the role of mir-148a-3p in crc cell proliferation and immune escape and its potential mechanism. mir-148a-3p and kruppel-like transcription factor 4 (klf4) expressions were quantified by western blot and quantitative real-time polymerase chain reaction (qrt-pcr). the proliferation, migration, invasion, epithelial-mesenchymal transition (emt), and immune evasion abilities of crc cells were evaluated with the cell counting kit-8 assay, transwell, western blot, and enzyme-linked immunosorbent assays. the proliferation or apoptosis of cd8+ and cd4+ t cells after coculture with crc cells was assessed by flow cytometry. dual-luciferase reporter gene testing was used to validate the targeting association between klf4 and mir-148a-3p. a nude mouse subcutaneous graft tumor model was constructed, and cd8+ t cell infiltration was detected by immunohistochemistry 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 cell proliferation, migration, invasion, emt, and immune escape; silencing mir-148a-3p caused the opposite trend; moreover, the said biological functions of crc cells were weakened with overexpression of klf4 but enhanced with silencing of klf4; silencing klf4 weakened the influences of dampened mir-148a-3p on crc development. silencing mir-148a-3p promoted the infiltration of cd8+ t cells and inhibited tumor growth.in summary, mir-148a-3p promotes crc cell proliferation and immune evasion by regulating the expression of klf4. this finding can be used for reference when developing a new way of crc treatment.