FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer
Abstract Background MicroRNAs (miRNAs) representing a subclass of non-coding RNAs are dynamically expressed and participate in multiple pathological responses, whereas, the expression pattern or function of miRNAs has not been fully addressed in triple-negative breast cancer (TNBC). Currently we con...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2020-05-01
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| Series: | Cancer Cell International |
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| Online Access: | http://link.springer.com/article/10.1186/s12935-020-01258-z |
| _version_ | 1818907455032131584 |
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| author | Purong Zhang Qimin Long Shiyan Zeng Min Wen Qing Lu |
| author_facet | Purong Zhang Qimin Long Shiyan Zeng Min Wen Qing Lu |
| author_sort | Purong Zhang |
| collection | DOAJ |
| description | Abstract Background MicroRNAs (miRNAs) representing a subclass of non-coding RNAs are dynamically expressed and participate in multiple pathological responses, whereas, the expression pattern or function of miRNAs has not been fully addressed in triple-negative breast cancer (TNBC). Currently we concentrate on dissecting the probable role of microRNA-663a (miR-663a) in TNBC cellular processes. Methods qRT-PCR detected the expression of miR-663a in TNBC cells. Besides, we monitored the effects of miR-663a on TNBC proliferation and apoptosis. On the basis of bioinformatics assistance and mechanical validation, we identified the miRNA-sponging role of LINC01123 and downstream target of miR-663a in TNBC was assessed and verified. The transcription activation of was explored via ChIP and luciferase reporter assays. Results In comparison to MCF-10A, we certified the downregulation of miR-663a in TNBC cell lines. Augmentation of miR-663a was anti-proliferation and pro-apoptosis in TNBC cell lines. LINC01123 protected CMIP against miR-663a suppression through acting as a sponge of miR-663a in TNBC. LINC01123 was transcriptionally induced by FOXC1. Rescue experiment proved that miR-663a suppression or CMIP (c-Maf inducing protein) enhancement could countervail LINC01123 depletion-mediated effects on TNBC cellular processes. Conclusion LINC01123, activated by FOXC1, regulated TNBC growth through miR-663a/CMIP signaling, which unveiled a new functional pathway of FOXC1-induced LINC01123/miR-663a/CMIP in TNBC. |
| first_indexed | 2024-12-19T21:55:23Z |
| format | Article |
| id | doaj.art-33ebc5365f6c46b98aec08ac5c75549c |
| institution | Directory Open Access Journal |
| issn | 1475-2867 |
| language | English |
| last_indexed | 2024-12-19T21:55:23Z |
| publishDate | 2020-05-01 |
| publisher | BMC |
| record_format | Article |
| series | Cancer Cell International |
| spelling | doaj.art-33ebc5365f6c46b98aec08ac5c75549c2022-12-21T20:04:17ZengBMCCancer Cell International1475-28672020-05-0120111510.1186/s12935-020-01258-zFOXC1-induced LINC01123 acts as a mediator in triple negative breast cancerPurong Zhang0Qimin Long1Shiyan Zeng2Min Wen3Qing Lu4Department of Breast Surgery, West China Hospital/West China School of Medicine, Sichuan UniversitySichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of ChinaSichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of ChinaSichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of ChinaDepartment of Breast Surgery, West China Hospital/West China School of Medicine, Sichuan UniversityAbstract Background MicroRNAs (miRNAs) representing a subclass of non-coding RNAs are dynamically expressed and participate in multiple pathological responses, whereas, the expression pattern or function of miRNAs has not been fully addressed in triple-negative breast cancer (TNBC). Currently we concentrate on dissecting the probable role of microRNA-663a (miR-663a) in TNBC cellular processes. Methods qRT-PCR detected the expression of miR-663a in TNBC cells. Besides, we monitored the effects of miR-663a on TNBC proliferation and apoptosis. On the basis of bioinformatics assistance and mechanical validation, we identified the miRNA-sponging role of LINC01123 and downstream target of miR-663a in TNBC was assessed and verified. The transcription activation of was explored via ChIP and luciferase reporter assays. Results In comparison to MCF-10A, we certified the downregulation of miR-663a in TNBC cell lines. Augmentation of miR-663a was anti-proliferation and pro-apoptosis in TNBC cell lines. LINC01123 protected CMIP against miR-663a suppression through acting as a sponge of miR-663a in TNBC. LINC01123 was transcriptionally induced by FOXC1. Rescue experiment proved that miR-663a suppression or CMIP (c-Maf inducing protein) enhancement could countervail LINC01123 depletion-mediated effects on TNBC cellular processes. Conclusion LINC01123, activated by FOXC1, regulated TNBC growth through miR-663a/CMIP signaling, which unveiled a new functional pathway of FOXC1-induced LINC01123/miR-663a/CMIP in TNBC.http://link.springer.com/article/10.1186/s12935-020-01258-zFOXC1LINC01123miR-663aCMIPTNBC |
| spellingShingle | Purong Zhang Qimin Long Shiyan Zeng Min Wen Qing Lu FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer Cancer Cell International FOXC1 LINC01123 miR-663a CMIP TNBC |
| title | FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer |
| title_full | FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer |
| title_fullStr | FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer |
| title_full_unstemmed | FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer |
| title_short | FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer |
| title_sort | foxc1 induced linc01123 acts as a mediator in triple negative breast cancer |
| topic | FOXC1 LINC01123 miR-663a CMIP TNBC |
| url | http://link.springer.com/article/10.1186/s12935-020-01258-z |
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