ArticleExperimental and therapeutic medicine2022
FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- FOXP Transcription Factors in Thyroid Cancer: From Molecular Expression to Clinical Significance.Biomedicines · 2026Review
- Mechanism of FOXP2 in the Hepatocellular Carcinoma Progression via Ferroptosis Through RBM15B-Mediated m6A Modification.Applied biochemistry and biotechnology · 2026Article
- FOXP2-Dependent Vulnerability of RGCs Under Acute Ocular Hypertension.Molecular neurobiology · 2025Article
- Two Cohorts, One Network: Consensus Master Regulators Orchestrating Papillary Thyroid Carcinoma.International journal of molecular sciences · 2025Article
- Effect of forkhead box protein P2-mediated activation of myosin light-chain kinase on the invasion and migration of endometrial cancer cells.CytoJournal · 2025Article
- FOXP2 inhibits the aggressiveness of lung cancer cells by blocking TGFβ signaling.Oncology letters · 2024Article
- TP53 mutation-related senescence is an indicator of hepatocellular carcinoma patient outcomes from multiomics profiles.Smart medicine · 2023Article
- Effect of FOXP2 transcription factor on immune infiltration of thyroid cancer and its potential clinical value.Frontiers in immunology · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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