4.5 Article

miR-124 regulates EMT based on ZEB2 target to inhibit invasion and metastasis in triple-negative breast cancer

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PATHOLOGY RESEARCH AND PRACTICE
卷 215, 期 4, 页码 697-704

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ELSEVIER GMBH
DOI: 10.1016/j.prp.2018.12.039

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miR-124; ZEB2; epithelial-mesenchymal transition; Triple-negative breast cancer; Invasion; Metastasis

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Background: Triple-negative breast cancer (TNBC) is highly invasive and aggressive and lacks specific molecular targets to improve the prognosis. MicroRNAs (miRNAs) serve a role in promoting and suppressing tumors in various types of malignant cancer, including TNBC. However, the regulatory mechanism of miR-124 in TNBC has still remains unclear. Methods: Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-124. Cell viability was analyzed with CCK-8 assay. Cell colony formation ability was detected with colony formation assay. Cell invasion was measured with transwell assay. Dual luciferase reporter assay was conducted to verify whether ZEB2 is a target gene of miR-124. The mRNA and protein expression levels of ZEB2 and EMT markers were detected by quantitative real time PCR and western blot, respectively. Results: Our results showed that miR-124 was down-regulated in TNBC tissues and cells. Overexpression of miR-124 inhibited the proliferation, metastasis and epithelial-mesenchymal transition (EMT) of TNBC cells. Furthermore, ZEB2 3'UTR was considered to be a direct target of miR-124 with luciferase reporter assay. Rescue experiments confirmed that EMT was regulated by miR-124 via suppression of ZEB2. Conclusion: miR-124 suppresses EMT and metastasis via ZEB2. Therefore, miR-124 may represent a potential therapeutic target for TNBC.

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