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Its specific role and mechanism in non\u2013small cell lung cancer (NSCLC) have not been reported yet. We prepared a cancer\u2010associated fibroblasts\u2010conditioned medium (CAF\u2010CM) to incubate the A549 cells. Quantitative real\u2010time polymerase chain reaction was used to detect RNA levels. We detected protein expression by immunohistochemistry, immunocytochemistry, western blot and immunofluorescence. We also detected the targeting impact between circFARP1, miR\u2010338\u20103p and SRY\u2010box transcription factor 4 (SOX4) by using dual\u2010luciferase reporter and RNA pull\u2010down assays. We determined cell proliferation, migration and invasion capabilities through Cell Counting Kit\u20108 and transwell assays. In addition, we measured tumour volume and weight in vivo by establishing a xenograft tumour model. CircFARP1 levels were remarkably high in the CAFs. The transfection experiments found that circFARP1 downregulation in CAFs caused migration, proliferation and invasion inhibition of CAFs and A549 cells, whereas inhibiting miR\u201038\u20103p or overexpressing SOX4 in CAFs could significantly reverse the inhibition. In vivo study in nude mice confirmed that CAFs could promote NSCLC tumour growth and knockdown of circFARP1 could inhibit tumour growth of NSCLC, whereas miR\u201038\u20103p downregulation or SOX4 overexpression could significantly reverse the inhibition. circFARP1 promotes NSCLC development by stimulating miR\u2010338\u20103p\/SOX4 signalling axis to regulate CAFs.<\/jats:p>","DOI":"10.1111\/1440-1681.13914","type":"journal-article","created":{"date-parts":[[2024,8,14]],"date-time":"2024-08-14T07:00:05Z","timestamp":1723618805000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Cancer\u2010associated fibroblast\u2010derived <scp>circFARP1<\/scp> modulates non\u2013small cell lung cancer invasion and metastasis through the <scp>circFARP1<\/scp>\/<scp>miR<\/scp>\u2010338\u20103p\/<scp>SOX4<\/scp> 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