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Background: Breast cancer is one of the most common cancers worldwide. Long non-coding RNAs and microRNAs act as important regulators in human cancers. This study aims to explore the molecular mechanism among H19, miR-491-5p and zinc finger 703 (ZNF703) in breast cancer.
Materials And Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect the expression of H19, miR-491-5p and ZNF703. Cell Counting Kit 8 (CCK-8) assay was performed to evaluate cell proliferation. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells was counted by transwell assay. Dual luciferase reporter assay was carried out to test luciferase activity. Protein level of ZNF703 was measured by Western blot assay.
Results: H19 was highly expressed in breast tissues and cells. H19 knockdown inhibited proliferation, induced apoptosis and blocked migration and invasion. Moreover, H19 bound to miR-491-5p and negatively regulated miR-491-5p expression. MiR-491-5p inhibition abrogated the activities of proliferation, apoptosis, migration and invasion affected by H19 knockdown. Furthermore, miR-491-5p directly targeted ZNF703 and inversely modulated ZNF703 expression. ZNF703 up-regulation rescued the effects of miR-491-5p overexpression on proliferation, apoptosis, migration and invasion. In addition, H19 knockdown reduced ZNF703 expression by targeting miR-491-5p/ZNF703 axis.
Conclusion: H19 promoted proliferation, migration and invasion and retarded apoptosis of breast cancer cells via sponging miR-491-5p to down-regulate ZNF703 expression.
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http://dx.doi.org/10.2147/CMAR.S246009 | DOI Listing |
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Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-Sur-Yvette, 91198, France.
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State Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Department of Radiology, Department of Clinical Research and Translational Medicine, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou,
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School of Life Sciences, Anhui Medical University, Hefei, 230032, China; Translational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metaboli
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View Article and Find Full Text PDFInt J Biol Macromol
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Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China; The Public Experimental Center of Medicine, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China. Electronic address: kexixian@z
Chemotherapy resistance in lung adenocarcinoma (LUAD) limits clinical efficacy. In this study, we first established circ_IGF2BP1 knockdown models in LUAD cells (A549 and H1299). Using dual-luciferase reporter assays, functional analyses, and miR-885-3p rescue experiments, we demonstrated that circ_IGF2BP1 promotes LUAD cell proliferation, migration, and invasion by directly targeting miR-885-3p.
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Department of Pathology, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, PR China; Department of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061, PR China. Electronic address:
Tumor-associated neutrophils (TANs) play a critical role in breast cancer progression. This study demonstrated that high CD66b TANs infiltration correlated with poor disease-free survival (DFS) and promoted proliferation, migration, and invasion of breast cancer cells in vitro. Conversely, the immune-related long non-coding RNA C6orf99 was downregulated in breast cancer and associated with favorable DFS.
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