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FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6

  • Authors:
    • Feibiao Yang
    • Zhangsheng Xiao
    • Songze Zhang
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    Affiliations: Department of Thyroid and Breast Surgery, The Affiliated People's Hospital of Ningbo University, Ningbo, Zhejiang 315040, P.R. China
    Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 434
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    Published online on: May 9, 2022
       https://doi.org/10.3892/etm.2022.11361
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Abstract

The transcription factor, forkhead box P2 (FOXP2) has tumor‑suppressive effects in several types of cancer. However, the regulatory role and underlying mechanism of FOXP2 in thyroid cancer (THCA) is not completely understood. In the present study, the mRNA expression levels of FOXP2 and ribosomal protein S6 kinase A6 (RPS6KA6) were evaluated using the GEPIA database and THCA cell lines. The association between FOXP2 and RPS6KA6 was analyzed using the LinkedOmics, and GEPIA databases. Then, the binding sites of FOXP2 and the RPS6KA6 promotor was predicted using the JASPAR database, and verified using a dual‑luciferase reporter assay and chromatin immunoprecipitation. In addition, functional assays investigating FOXP2 and RPS6KA6 were conducted in the TPC‑1 cell line. The data showed that FOXP2 and RPS6KA6 mRNA expression levels were decreased in the THCA tissues, and cell lines. Overexpression of FOXP2 inhibited cell proliferation and promoted apoptosis in the THCA cell lines. Furthermore, RPS6KA6 mRNA expression levels were reduced in THCA and were correlated with FOXP2 expression level. Mechanistic studies revealed that FOXP2 binds directly to the promotor region of RPS6KA6 and modulated the expression level of RPS6KA6 transcriptionally. In addition, rescue experiments showed that knockdown of RPS6KA6 expression reversed the effects of FOXP2 overexpression on THCA cell proliferation and apoptosis, and the regulation of FOXP2/RPS6KA6 may be associated with the PI3K/AKT pathway. In summary, FOXP2 was associated with the proliferation and apoptosis of human THCA cells via the transcriptional activation of RPS6KA6. The FOXP2/RPS6KA6 axis could be a promising target for the treatment of THCA.
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Copy and paste a formatted citation
Spandidos Publications style
Yang F, Xiao Z and Zhang S: FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6. Exp Ther Med 23: 434, 2022.
APA
Yang, F., Xiao, Z., & Zhang, S. (2022). FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6. Experimental and Therapeutic Medicine, 23, 434. https://doi.org/10.3892/etm.2022.11361
MLA
Yang, F., Xiao, Z., Zhang, S."FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6". Experimental and Therapeutic Medicine 23.6 (2022): 434.
Chicago
Yang, F., Xiao, Z., Zhang, S."FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6". Experimental and Therapeutic Medicine 23, no. 6 (2022): 434. https://doi.org/10.3892/etm.2022.11361
Copy and paste a formatted citation
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Spandidos Publications style
Yang F, Xiao Z and Zhang S: FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6. Exp Ther Med 23: 434, 2022.
APA
Yang, F., Xiao, Z., & Zhang, S. (2022). FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6. Experimental and Therapeutic Medicine, 23, 434. https://doi.org/10.3892/etm.2022.11361
MLA
Yang, F., Xiao, Z., Zhang, S."FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6". Experimental and Therapeutic Medicine 23.6 (2022): 434.
Chicago
Yang, F., Xiao, Z., Zhang, S."FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6". Experimental and Therapeutic Medicine 23, no. 6 (2022): 434. https://doi.org/10.3892/etm.2022.11361
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