Background and Aims Long non-coding RNAs (lncRNAs) can indirectly regulate the transcription and degradation of downstream mRNAs by binding to microRNAs (miRNAs), thereby regulating the occurrence and development of tumors. LncRNA FOXP4-AS1 is a recently discovered tumor-related biomarker, playing different regulatory roles in different tumors. Our previous study found that FOXP4-AS1 is downregulated in papillary thyroid carcinoma (PTC) and is a tumor suppressor. In addition, bioinformatics analysis predicted that miR-507 could complementarily bind to FOXP4-AS1. Therefore, this study was conducted to explore the role and mechanism of FOXP4-AS1 in inhibiting the growth of PTC cells by regulating miR-507 and its downstream target mRNA.Methods The expression levels of miR-507 in thyroid cancer (TC) and its clinical significance were analyzed using the TCGA database. The expression levels of miR-507 in PTC cell lines (TPC-1, K1) and normal thyroid follicular epithelial cells (Nthy-ori3-1) were detected by qRT-PCR and the changes in miR-507 expression levels after overexpression and knockdown of FOXP4-AS1 were measured. The dual-luciferase reporter gene assay was used to verify the targeting relationship between FOXP4-AS1 and miR-507. miR-507 mimic and inhibitor were transfected into stable cell lines overexpressing or knockdown of FOXP4-AS1, and changes in cell function were detected by CCK-8 assay, colony formation assay, Transwell assay, scratch healing assay, and flow cytometry. Bioinformatics analysis was used to predict the downstream targets of miR-507, and qRT-PCR was used for validation.Results Analysis of the TCGA database showed that miR-507 was highly expressed in TC, and its expression level was associated with clinical pathological features such as clinical stage, T stage, and extrathyroidal infiltration (all P<0.05). qRT-PCR results showed that compared with Nthy-ori3-1 cells, miR-507 was highly expressed in both PTC cell lines, and the expression levels of miR-507 in both PTC cells changed inversely after overexpression and knockdown of FOXP4-AS1 (all P<0.05). The results of the dual-luciferase reporter gene assay showed that FOXP4-AS1 targeted and inhibited the expression of miR-507. Cell function experiments and functional recovery experiments showed that after overexpression of FOXP4-AS1, the proliferation, migration, and anti-apoptotic ability of PTC cells were significantly weakened, and these functions were restored after the addition of miR-507 mimic (all P<0.05); knockdown of FOXP4-AS1 in PTC cells resulted in a significant increase in proliferation, migration, and anti-apoptotic ability, and these functions were restored after the addition of the miR-507 inhibitor (all P<0.05). Bioinformatics prediction and GO, KEGG enrichment analysis results showed that miR-507 downstream may involve CAMK4. qRT-PCR validation results showed that the expression level of CAMK4 changed in the same direction as the expression level of FOXP4-AS1, and its expression level changed inversely with the addition of miR-507 mimic and inhibitor (all P<0.05).Conclusion FOXP4-AS1 can target miR-507, and may regulate the proliferation, migration, and apoptosis of PTC cells by inhibiting the expression level of miR-507 through a sponge mechanism. CAMK4 may be one of the downstream targets of the FOXP4-AS1/miR-507 pathway in exerting its anticancer effects.