MiR-16-5p suppresses breast cancer proliferation by targeting ANLN
Abstract Background In recent years, gene expression-based analysis has been used for disease biomarker discovery, providing ways for better diagnosis, leading to improvement of clinical treatment efficacy. This study aimed to explore the role of miR-16-5p and ANLN in breast cancer (BC). Methods Coh...
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| Format: | Article |
| Language: | English |
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BMC
2021-11-01
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| Series: | BMC Cancer |
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| Online Access: | https://doi.org/10.1186/s12885-021-08914-1 |
| _version_ | 1818926774596141056 |
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| author | Ziming Wang Siyuan Hu Xinyang Li Zhiwei Liu Danyang Han Yukun Wang Limin Wei Guangping Zhang Xinshuai Wang |
| author_facet | Ziming Wang Siyuan Hu Xinyang Li Zhiwei Liu Danyang Han Yukun Wang Limin Wei Guangping Zhang Xinshuai Wang |
| author_sort | Ziming Wang |
| collection | DOAJ |
| description | Abstract Background In recent years, gene expression-based analysis has been used for disease biomarker discovery, providing ways for better diagnosis, leading to improvement of clinical treatment efficacy. This study aimed to explore the role of miR-16-5p and ANLN in breast cancer (BC). Methods Cohort datasets of BC were obtained from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) and analyzed by bioinformatics tools. qRT-PCR and western blotting were applied to validate ANLN and its protein expression. A dual-luciferase reporter assay was used to prove the regulatory relationship of miR-16-5p and ANLN. Finally, MTT, wound healing, Transwell invasion and flow cytometry analyses of the cell cycle and apoptosis were performed to assess cell proliferation, migration, invasion, cell cycle and apoptosis, respectively. Results A total of 195 differentially expressed genes (DEGs) and 50 overlapping microRNAs (miRNAs) were identified. Among these DEGs and miRNAs, ANLN, associated with poor overall survival in BC, overlapped in the GSE29431, GSE42568, TCGA and GEPIA2 databases. Moreover, ANLN was highly expressed, while miR-16-5p was lower in BC cells than in breast epithelial cells. Then, we confirmed that ANLN was directly targeted by miR-16-5p in BC cells. Over-expression of miR-16-5p and knock-down of ANLN remarkably inhibited cell proliferation and migration as well as cell invasion, arrested the cells in G2/M phase and induced apoptosis in BC cells. Conclusions These findings suggest that miR-16-5p restrains proliferation, migration and invasion while affecting cell cycle and promotes apoptosis by regulating ANLN, thereby providing novel candidate biomarkers for the diagnosis and treatment of BC. |
| first_indexed | 2024-12-20T03:02:28Z |
| format | Article |
| id | doaj.art-0208350eaf2f41979c3f171f9a6928a8 |
| institution | Directory Open Access Journal |
| issn | 1471-2407 |
| language | English |
| last_indexed | 2024-12-20T03:02:28Z |
| publishDate | 2021-11-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Cancer |
| spelling | doaj.art-0208350eaf2f41979c3f171f9a6928a82022-12-21T19:55:42ZengBMCBMC Cancer1471-24072021-11-0121111210.1186/s12885-021-08914-1MiR-16-5p suppresses breast cancer proliferation by targeting ANLNZiming Wang0Siyuan Hu1Xinyang Li2Zhiwei Liu3Danyang Han4Yukun Wang5Limin Wei6Guangping Zhang7Xinshuai Wang8Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyZhoukou first people’s HospitalHenan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyHenan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyHenan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyHenan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyHenan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyHenan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyHenan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and TechnologyAbstract Background In recent years, gene expression-based analysis has been used for disease biomarker discovery, providing ways for better diagnosis, leading to improvement of clinical treatment efficacy. This study aimed to explore the role of miR-16-5p and ANLN in breast cancer (BC). Methods Cohort datasets of BC were obtained from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) and analyzed by bioinformatics tools. qRT-PCR and western blotting were applied to validate ANLN and its protein expression. A dual-luciferase reporter assay was used to prove the regulatory relationship of miR-16-5p and ANLN. Finally, MTT, wound healing, Transwell invasion and flow cytometry analyses of the cell cycle and apoptosis were performed to assess cell proliferation, migration, invasion, cell cycle and apoptosis, respectively. Results A total of 195 differentially expressed genes (DEGs) and 50 overlapping microRNAs (miRNAs) were identified. Among these DEGs and miRNAs, ANLN, associated with poor overall survival in BC, overlapped in the GSE29431, GSE42568, TCGA and GEPIA2 databases. Moreover, ANLN was highly expressed, while miR-16-5p was lower in BC cells than in breast epithelial cells. Then, we confirmed that ANLN was directly targeted by miR-16-5p in BC cells. Over-expression of miR-16-5p and knock-down of ANLN remarkably inhibited cell proliferation and migration as well as cell invasion, arrested the cells in G2/M phase and induced apoptosis in BC cells. Conclusions These findings suggest that miR-16-5p restrains proliferation, migration and invasion while affecting cell cycle and promotes apoptosis by regulating ANLN, thereby providing novel candidate biomarkers for the diagnosis and treatment of BC.https://doi.org/10.1186/s12885-021-08914-1Breast cancerBioinformaticsANLNmiR-16-5pProliferation |
| spellingShingle | Ziming Wang Siyuan Hu Xinyang Li Zhiwei Liu Danyang Han Yukun Wang Limin Wei Guangping Zhang Xinshuai Wang MiR-16-5p suppresses breast cancer proliferation by targeting ANLN BMC Cancer Breast cancer Bioinformatics ANLN miR-16-5p Proliferation |
| title | MiR-16-5p suppresses breast cancer proliferation by targeting ANLN |
| title_full | MiR-16-5p suppresses breast cancer proliferation by targeting ANLN |
| title_fullStr | MiR-16-5p suppresses breast cancer proliferation by targeting ANLN |
| title_full_unstemmed | MiR-16-5p suppresses breast cancer proliferation by targeting ANLN |
| title_short | MiR-16-5p suppresses breast cancer proliferation by targeting ANLN |
| title_sort | mir 16 5p suppresses breast cancer proliferation by targeting anln |
| topic | Breast cancer Bioinformatics ANLN miR-16-5p Proliferation |
| url | https://doi.org/10.1186/s12885-021-08914-1 |
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