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Objective: Thyroid cancer (THCA) is the most common endocrine cancer in the world. Although most patients with THCA have a good prognosis, the prognosis of those with THCA who have an extra-glandular invasion, vascular invasion, and distant metastasis is poor. Therefore, it is very important to find potential bioma rkers that can effectively predict the prognosis and progression of highly aggressive THCA s. It has been identified that forkhead box P4 (FOXP4) may be a new biomarker for the pro liferation and prognosis for tumor diagnosis. However, the expression and function of FOXP4 in THCA remain to be determined. Methods: In the present study, the function of FOXP4 in cells was investigated through the comprehensive analysis of data in The Cancer Genome Atlas and combined with experiments including immunohistochemistry (IHC), colony formation, Cell Counting Kit-8 assay, wound scratch healing, and transwell invasion assay. Results: In the present study, relevant bioinformatic data showed that FOXP4 was highly expressed in THCA, which was consistent with the results of the IHC and cell experiments. Meanwhile, 10 FOXP4-related hub genes were identifi ed as potential diagnostic genes for THCA. It was found in further experiments that FOXP4 was located in the nucleus of THCA cells, and the expression of FOXP4 in the nucleus was higher than that in the cytoplasm. FOXP4 knockdown inhibited in vitro proliferation of the THCA cells, whereas overexpression promoted the proliferation and migration of THCA cells. Furthermore, deficiency of FOXP4 induced cell-cycle arrest. Conclusion: FOXP4 might be a potential target for diagnosing and treating THCA.

Esophageal squamous cell carcinoma (ESCC) belongs to one of the most common malignant tumors worldwide and possesses high mortality. Long non‐coding RNAs (lncRNAs) have been demonstrated to be essential biological participants in the progression of ESCC. On the basis of bio‐informatics prediction, forkhead box P4 antisense RNA 1 (FOXP4‐AS1) and forkhead box P4 (FOXP4) were upregulated in esophageal carcinoma samples and were positively correlated with each other. The present study aimed to explore the function of FOXP4‐AS1 and FOXP4 in ESCC cells. Function assays disclosed that knockdown of FOXP4‐AS1 or FOXP4 efficiently suppressed cell proliferation and induced cell apoptosis. Moreover, FOXP4‐AS1 positively regulated FOXP4 by interacting with insulin‐like growth factor 2 mRNA‐binding protein 2 (IGF2BP2) to stabilize FOXP4 messenger RNA. In addition, FOXP4‐AS1 could upregulate the expression of FOXP4 by sponging miR‐3184‐5p. Finally, we found that Yin Yang 1 (YY1) is a transcription factor that can transcriptionally activate both FOXP4‐AS1 and FOXP4 in ESCC cells. In a word, YY1‐induced upregulation of FOXP4‐AS1 and FOXP4 promote the proliferation of ESCC cells [ABSTRACT FROM AUTHOR]

In recent years, circular RNAs (circRNAs) have been identified to be essential regulators of various human cancers. However, knowledge of the functions of circRNAs in prostate cancer remains very limited. The correlation between circABCC4 and human cancer is largely unknown. This study aims to investigate the biological functions of circABCC4 in prostate cancer progression and illustrate the underlying mechanism. We found that circABCC4 was remarkably up‐regulated in prostate cancer tissues and cell lines and promoted FOXP4 expression by sponging miR‐1182 in prostate cancer cells. CircABCC4 knockdown markedly suppressed prostate cancer cell proliferation, cell‐cycle progression, migration and invasion in vitro. Furthermore, silencing of the circRNA also delayed tumor growth in vivo. Taken together, our findings indicated that circABCC4 facilitates the malignant behaviour of prostate cancer by promoting FOXP4 expression through sponging of miR‐1182. The circABCC4–miR‐1182‐FOXP4 regulatory loop may be a promising therapeutic target for prostate cancer intervention. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that FoxP1, FoxP2 and FoxP3 play important roles in hepatocellular carcinoma (HCC). However, the effect of FoxP4 in HCC requires further elucidation. The aim of the present study was to explore the roles of FoxP4 in HCC and further decipher the detailed mechanism. In present study, it was found that FoxP4, which is overexpressed in HCC tissues and cell lines, facilitated EMT in HCC cell lines through regulation of Slug. First, increased expression of FoxP4 was identified in 110 pairs of human HCC tumor and their adjacent normal tissues. In addition, the association between FoxP4 expression and clinicopathological features of HCC patients indicated that FoxP4 played vital roles in HCC development. Subsequently, gain- and loss-of-function experiments indicated that FoxP4 promoted cellular proliferation, migration as well invasion. In addition, EMT, a key mechanism during cancer metastasis, was regulated by FoxP4. Furthermore, ChIP and qChIP as well as luciferase reporter assays indicated that Slug, an EMT-associated transcription factor, was transcriptionally regulated by FoxP4. In conclusion, FoxP4 functioned as a tumor promoter in HCC cells by transcriptionally regulating Slug, and the present study highlighted the potential effects of FoxP4 on the prognosis and treatment of HCC. [ABSTRACT FROM AUTHOR]

Recently, circular RNAs (circRNAs) have been demonstrated as essential regulators in human cancers. However, the function and mechanism of circRNAs in breast cancer (BC) remain largely unknown and require to be investigated. In the present study, we found that circMYO9B was highly expressed in BC tissues by bioinformatics analysis. And we showed that circMYO9B expression was positively correlated with patients' prognosis. Moreover, we found that circMYO9B knockdown significantly suppressed the proliferation, migration and invasion of BC cells in vitro . In vivo assays also indicated that circMYO9B silence delayed tumor growth. In mechanism, we found that circMYO9B promoted the expression of FOXP4 by sponging miR-4316 in BC cells. We showed that the expression of miR-4316 was inversely associated with that of circMYO9B or FOXP4 in BC tissues. Finally, we found that restoration of FOXP4 expression significantly reversed the effects of circMYO9B knockdown on BC cell proliferation, migration and invasion. In conclusion, our findings demonstrated a key role of circMYO9B/miR-4316/FOXP4 axis in regulating BC progression. [ABSTRACT FROM AUTHOR]