Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-catenin
Background Recent studies have found that circular RNAs (circRNAs) play important roles in tumorigenesis. This study aimed to determine the function and potential mechanisms of hsa_circ_0001615 in esophageal cancer. Methods Quantitative real-time reverse transcription polymerase chain reaction (qRT-...
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PeerJ Inc.
2024-03-01
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| Online Access: | https://peerj.com/articles/17089.pdf |
| _version_ | 1797270196068548608 |
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| author | Yukai Dai Qizhong Xu Manqi Xia Caimin Chen Xinming Xiong Xin Yang Wei Wang |
| author_facet | Yukai Dai Qizhong Xu Manqi Xia Caimin Chen Xinming Xiong Xin Yang Wei Wang |
| author_sort | Yukai Dai |
| collection | DOAJ |
| description | Background Recent studies have found that circular RNAs (circRNAs) play important roles in tumorigenesis. This study aimed to determine the function and potential mechanisms of hsa_circ_0001615 in esophageal cancer. Methods Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was used to validate the expression of hsa_circ_0001615 and miR-142-5p. Subsequently, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt, flow cytometry, clone formation, and transwell assays were used to assess the function of hsa_circ_0001615. Furthermore, qRT-PCR and Western blot analysis were used to verify cyclin D1, Bcl-2 associated X, B-cell lymphoma/leukemia gene-2, and β-catenin levels. Circular RNA Interactome was used to estimate the binding site between hsa_circ_0001615 and miR-142-5p. Additionally, dual-luciferase reporter assays were used to determine whether miR-142-5p was a direct target of hsa_circ_0001615. Pearson correlation analysis was used to explore the relationship between miR-142-5p and hsa_circ_0001615. Results In esophageal cancer, the expressions of hsa_circ_0001615 and miR-142-5p were increased and decreased, respectively. Hsa_circ_0001615 inhibition significantly reduced the proliferation, migration, and invasion but increased the apoptosis of esophageal cancer cells. Additionally, hsa_circ_0001615 knockdown increased miR-142-5p expression but decreased β-catenin expression. MiR-142-5p was a direct target of hsa_circ_0001615. Conclusion Hsa_circ_0001615 knockdown could mediate antitumor effects through the miR-142-5p/β-catenin pathway. |
| first_indexed | 2024-04-25T02:00:25Z |
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| language | English |
| last_indexed | 2024-04-25T02:00:25Z |
| publishDate | 2024-03-01 |
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| spelling | doaj.art-3f0087ff573142a79ff8a0e4e3f498d62024-03-07T15:05:15ZengPeerJ Inc.PeerJ2167-83592024-03-0112e1708910.7717/peerj.17089Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-cateninYukai Dai0Qizhong Xu1Manqi Xia2Caimin Chen3Xinming Xiong4Xin Yang5Wei Wang6The Second Clinical College of Guangzhou Medical University, Guangzhou, ChinaThe Second Clinical College of Guangzhou Medical University, Guangzhou, ChinaThe Second Clinical College of Guangzhou Medical University, Guangzhou, ChinaThe Second Clinical College of Guangzhou Medical University, Guangzhou, ChinaThe Second Clinical College of Guangzhou Medical University, Guangzhou, ChinaThe Second Clinical College of Guangzhou Medical University, Guangzhou, ChinaThe Second Clinical College of Guangzhou Medical University, Guangzhou, ChinaBackground Recent studies have found that circular RNAs (circRNAs) play important roles in tumorigenesis. This study aimed to determine the function and potential mechanisms of hsa_circ_0001615 in esophageal cancer. Methods Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was used to validate the expression of hsa_circ_0001615 and miR-142-5p. Subsequently, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt, flow cytometry, clone formation, and transwell assays were used to assess the function of hsa_circ_0001615. Furthermore, qRT-PCR and Western blot analysis were used to verify cyclin D1, Bcl-2 associated X, B-cell lymphoma/leukemia gene-2, and β-catenin levels. Circular RNA Interactome was used to estimate the binding site between hsa_circ_0001615 and miR-142-5p. Additionally, dual-luciferase reporter assays were used to determine whether miR-142-5p was a direct target of hsa_circ_0001615. Pearson correlation analysis was used to explore the relationship between miR-142-5p and hsa_circ_0001615. Results In esophageal cancer, the expressions of hsa_circ_0001615 and miR-142-5p were increased and decreased, respectively. Hsa_circ_0001615 inhibition significantly reduced the proliferation, migration, and invasion but increased the apoptosis of esophageal cancer cells. Additionally, hsa_circ_0001615 knockdown increased miR-142-5p expression but decreased β-catenin expression. MiR-142-5p was a direct target of hsa_circ_0001615. Conclusion Hsa_circ_0001615 knockdown could mediate antitumor effects through the miR-142-5p/β-catenin pathway.https://peerj.com/articles/17089.pdfHsa_circ_0001615miR-142-5pEsophageal cancerβ-catenin |
| spellingShingle | Yukai Dai Qizhong Xu Manqi Xia Caimin Chen Xinming Xiong Xin Yang Wei Wang Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-catenin PeerJ Hsa_circ_0001615 miR-142-5p Esophageal cancer β-catenin |
| title | Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-catenin |
| title_full | Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-catenin |
| title_fullStr | Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-catenin |
| title_full_unstemmed | Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-catenin |
| title_short | Hsa_circ_0001615 downregulation inhibits esophageal cancer development through miR-142-5p/β-catenin |
| title_sort | hsa circ 0001615 downregulation inhibits esophageal cancer development through mir 142 5p β catenin |
| topic | Hsa_circ_0001615 miR-142-5p Esophageal cancer β-catenin |
| url | https://peerj.com/articles/17089.pdf |
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