BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progression
Abstract Background Papillary thyroid carcinoma (PTC) is a common malignant tumor. BRAFV600E mutation has become a common molecular event in PTC pathogenesis. Circular RNA PSD3 (circPSD3) is known to be highly expressed in PTC. However, the bio-functional role of circPSD3 and its possible relationsh...
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2025-01-01
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author | Chuang Li Xiaojuan Zhao Jingge Zhao Jing Zhao Lemei An Gang Wu |
author_facet | Chuang Li Xiaojuan Zhao Jingge Zhao Jing Zhao Lemei An Gang Wu |
author_sort | Chuang Li |
collection | DOAJ |
description | Abstract Background Papillary thyroid carcinoma (PTC) is a common malignant tumor. BRAFV600E mutation has become a common molecular event in PTC pathogenesis. Circular RNA PSD3 (circPSD3) is known to be highly expressed in PTC. However, the bio-functional role of circPSD3 and its possible relationship with the BRAF in PTC is not clear. This study aims to probe the biofunction and molecular mechanism of circPSD3 in PTC pathogenesis. Methods RT-qPCR was utilized to measure the expression of circPSD3 and BRAF in PTC tissues and cells. The CCK-8 and EdU assays were employed to assess cell viability and proliferation. Cell apoptosis was quantified using flow cytometry. The migratory and invasive capabilities of the cells were evaluated via wound healing and transwell assays. The interaction between RNAs was investigated using luciferase reporter assay. Additionally, xenograft tumor experiments were conducted to validate our findings in vivo. Results Data showed that circPSD3 was highly expressed in PTC patients and cell lines. CircPSD3 was found to promote cell growth and migration and inhibit apoptosis in PTC cells. Results also revealed that circPSD3 upregulated RAP2A expression by specifically sponging miR-526b. Interestingly, inhibiting miR-526b reversed the tumorigenic properties of circPSD3 in PTC. Additionally, BRAF expression was low in PTC patients, and overexpression of BRAF hampered PTC development by downregulating circPSD3 and RAP2A while upregulating miR-526b expressions. Conclusions Our study reveals that circPSD3 is a key regulator promoting PTC progression via the circPSD3/miR-526b/RAP2A pathway. Furthermore, we found that overexpressing BRAF, which inhibits circPSD3, significantly hampers the progression of PTC. |
format | Article |
id | doaj-art-b01d62d68a364783a3d7d57ab08b7d80 |
institution | Kabale University |
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language | English |
publishDate | 2025-01-01 |
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series | BMC Molecular and Cell Biology |
spelling | doaj-art-b01d62d68a364783a3d7d57ab08b7d802025-01-26T12:57:38ZengBMCBMC Molecular and Cell Biology2661-88502025-01-0126111510.1186/s12860-024-00528-2BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progressionChuang Li0Xiaojuan Zhao1Jingge Zhao2Jing Zhao3Lemei An4Gang Wu5Department of Ultrasound, Henan Provincial People’s HospitalDepartment of Ultrasound, Henan Provincial People’s HospitalDepartment of Clinical Scientific Research Service Center, Henan Provincial People’s HospitalDepartment of Ultrasound, Henan Provincial People’s HospitalDepartment of Rheumatology and Immunology, Henan Provincial People’s HospitalDepartment of Ultrasound, Henan Provincial People’s HospitalAbstract Background Papillary thyroid carcinoma (PTC) is a common malignant tumor. BRAFV600E mutation has become a common molecular event in PTC pathogenesis. Circular RNA PSD3 (circPSD3) is known to be highly expressed in PTC. However, the bio-functional role of circPSD3 and its possible relationship with the BRAF in PTC is not clear. This study aims to probe the biofunction and molecular mechanism of circPSD3 in PTC pathogenesis. Methods RT-qPCR was utilized to measure the expression of circPSD3 and BRAF in PTC tissues and cells. The CCK-8 and EdU assays were employed to assess cell viability and proliferation. Cell apoptosis was quantified using flow cytometry. The migratory and invasive capabilities of the cells were evaluated via wound healing and transwell assays. The interaction between RNAs was investigated using luciferase reporter assay. Additionally, xenograft tumor experiments were conducted to validate our findings in vivo. Results Data showed that circPSD3 was highly expressed in PTC patients and cell lines. CircPSD3 was found to promote cell growth and migration and inhibit apoptosis in PTC cells. Results also revealed that circPSD3 upregulated RAP2A expression by specifically sponging miR-526b. Interestingly, inhibiting miR-526b reversed the tumorigenic properties of circPSD3 in PTC. Additionally, BRAF expression was low in PTC patients, and overexpression of BRAF hampered PTC development by downregulating circPSD3 and RAP2A while upregulating miR-526b expressions. Conclusions Our study reveals that circPSD3 is a key regulator promoting PTC progression via the circPSD3/miR-526b/RAP2A pathway. Furthermore, we found that overexpressing BRAF, which inhibits circPSD3, significantly hampers the progression of PTC.https://doi.org/10.1186/s12860-024-00528-2Papillary thyroid carcinomacircRNAsmiRNAsPathogenesisMechanism |
spellingShingle | Chuang Li Xiaojuan Zhao Jingge Zhao Jing Zhao Lemei An Gang Wu BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progression BMC Molecular and Cell Biology Papillary thyroid carcinoma circRNAs miRNAs Pathogenesis Mechanism |
title | BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progression |
title_full | BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progression |
title_fullStr | BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progression |
title_full_unstemmed | BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progression |
title_short | BRAF regulates circPSD3/miR-526b/RAP2A axis to hinder papillary thyroid carcinoma progression |
title_sort | braf regulates circpsd3 mir 526b rap2a axis to hinder papillary thyroid carcinoma progression |
topic | Papillary thyroid carcinoma circRNAs miRNAs Pathogenesis Mechanism |
url | https://doi.org/10.1186/s12860-024-00528-2 |
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