miR-129-2 suppresses proliferation and migration of esophageal carcinoma cells through downregulation of SOX4 expression

Kang, Min; Li, Yumei; Liu, Wenqi; Wang, Rensheng; Tang, Anzhou; Hao, Hong; Liu, Zhenguo; Ou, Hesheng

doi:10.3892/ijmm.2013.1384

Cited by 68 publications

(57 citation statements)

References 40 publications

(43 reference statements)

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“…Previous studies have revealed that protein levels of Sox4 were controlled by several miRNAs, such as miR-129-2, miR-138, miR-203 and miR-204 [23,24,25,26]. Although the reason why multiple microRNAs regulate a single mRNA remains poorly understood until now, our study together with these reports add a novel mechanism for the up-regulation of Sox4 in human cancers.…”

Section: Discussionmentioning

confidence: 63%

MicroRNA-212 Inhibits Osteosarcoma Cells Proliferation and Invasion by Down-Regulation of Sox4

Luο

Tang

Gao

et al. 2014

Cell Physiol Biochem

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Background: Multiple MicroRNAs (miRNAs) have been identified in the development and progression of osteosarcoma. However, the expression and roles of miR-212 in osteosarcoma remain largely undefined. Methods: Real-time PCR assays were used to detect the expression of miR-212 in human osteosarcoma tissues. MiR-212 mimics were introduced into MG63 and U2OS cells. Bioinformatic prediction was used to identify the potential targets of miR-212. Protein expression analysis, luciferase assays and rescue assays were used to confirm the substrate of miR-212. Results: miR-212 was significantly down-regulated in human osteosarcoma tissues, compared with adjacent normal tissues. Introduction of miR-212 mimics into MG63 and U2OS cells inhibited cell proliferation and invasion. Besides, miR-212 overexpression could also inhibit tumor growth in the nude mice. Additionally, bioinformatic prediction suggested that the sex-determining region Y-box 4 (Sox4) is a target gene of miR-212. Sox4 inhibition phenocopied the roles of miR-212, while restored expression of Sox4 dampened miR-212-mediated suppression of tumor progression. Conclusion: The miR-212/Sox4 interaction plays an important role of in the osteosarcoma progression.

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Section: Discussionmentioning

confidence: 63%

MicroRNA-212 Inhibits Osteosarcoma Cells Proliferation and Invasion by Down-Regulation of Sox4

Luο

Tang

Gao

et al. 2014

Cell Physiol Biochem

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“…microRNAs have emerged as key regulators of the immune system, including regulation of cell cycle (miR-34c, miR-138, miR-193b, miR-129, and let-7f), induction of innate immunity (let-7f, miR-146b, miR-155, miR-192, miR-223, miR-451), and the development and differentiation of B and T cells (miR-34c, miR-181a, miR17-92 cluster) (4,10,17,20,26,45,50,52,53).…”

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confidence: 99%

microRNAs Regulate Host Immune Response and Pathogenesis During Influenza Infection in Rhesus Macaques

et al. 2016

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microRNAs (miRNAs) are small noncoding RNAs that are key regulators of biological processes, including the immune response to viral infections. Differential expression levels of cellular miRNAs and their predicted targets have been described in the lungs of H1N1-infected BALB/c mice, the lungs of H5N1 influenza-infected cynomolgus macaques, and in peripheral blood mononuclear cells (PBMCs) of critically ill patients infected with 2009 pandemic H1N1. However, a longitudinal analysis of changes in the expression of miRNAs and their targets during influenza infection and how they relate to viral replication and host response has yet to be carried out. In the present study, we conducted a comprehensive analysis of innate and adaptive immune responses as well as the expression of several miRNAs and their validated targets in both peripheral blood and bronchoalveolar lavage (BAL) collected from rhesus macaques over the course of infection with the 2009 H1N1 virus A/Mexico/4108/2009 (MEX4108). We describe a distinct set of differentially expressed miRNAs in BAL and PBMCs, which regulate the expression of genes involved in inflammation, immune response, and regulation of cell cycle and apoptosis.

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“…However, their 3'-prime products are different, which are named miR-129-1-3p and miR-129-2-3p, respectively (6,7). Dysregulation of miR-129-2 is frequently detected in solid tumors (8)(9)(10)(11)(12)(13). However, the role of miR-129-2 in breast cancer remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miR-129-2 by promoter hypermethylation regulates breast cancer cell proliferation and apoptosis

Tang

Liu

et al. 2016

Oncology Reports

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Abstract. Aberrant expression of the miR-129 family has been found in several types of cancer, yet its expression and potential biologic role in breast cancer remain largely unknown. In the present study, we found that miR-129-2 was consistently downregulated in the breast cancer specimens and cell lines. Overexpression of miR-129-2-3p markedly suppressed breast cancer cell proliferation and induced its apoptosis. In addition, a luciferase reporter assay revealed that miR-129-2-3p suppressed BCL2L2 expression. Furthermore, BCL2L2 was able to reverse miR-129-2-3p-mediated cell apoptosis, indicating that BCL2L2 plays a crucial role in mediating the tumor-suppressive role of miR-129-2-3p. Moreover, bisulfite DNA sequencing PCR (BSP) analysis identified that promoter hypermethylation was responsible for the downregulation of miR-129-2 in breast cancer. Collectively, our findings indicate that miR-129-2 is downregulated in breast cancer cells by promoter hypermethylation. Moreover, downregulation of miR-129-2 results in BCL2L2 overexpression and disease progression in breast cancer patients.

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miR-129-2 suppresses proliferation and migration of esophageal carcinoma cells through downregulation of SOX4 expression

Cited by 68 publications

References 40 publications

MicroRNA-212 Inhibits Osteosarcoma Cells Proliferation and Invasion by Down-Regulation of Sox4

MicroRNA-212 Inhibits Osteosarcoma Cells Proliferation and Invasion by Down-Regulation of Sox4

microRNAs Regulate Host Immune Response and Pathogenesis During Influenza Infection in Rhesus Macaques

Downregulation of miR-129-2 by promoter hypermethylation regulates breast cancer cell proliferation and apoptosis

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