MiR-129-2 functions as a tumor suppressor in glioma cells by targeting HMGB1 and is down-regulated by DNA methylation

Yu, Yang; Huang, Junqiang; Zhang, Xi; Shen, Liangfang

doi:10.1007/s11010-015-2382-6

Cited by 59 publications

(50 citation statements)

References 39 publications

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“…In glioma cells, miR-129-2 could function as a tumor suppressor by targeting HMGB1. Reintroducing of miR-129-2 suppressed cell growth [46]. Consistently, restoration of miR-129-2 restrained glioma cell proliferation partially through repressing of some major oncogenic genes, such as PDGFRa and Foxp1 [47].…”

Section: Mir-129 and Cell Proliferationmentioning

confidence: 66%

“…In addition, the hypermethylation of the CpG island upstream of miR-129-2 in glioma patients led to the down-regulation of miR-129-2 by targeting HMGB1. Besides, demethylation of miR-129-2 by 5-Aza-dC treatment augmented miR-129-2 expression in glioma cells [46]. Several other studies also demonstrated that the downregulation of miR-129-2 was generally through chromatin remodeling and DNA methylation in glioma cells, and miR-129-2 expression could be restored upon treatment with trichostatin A (a histone deadetylase inhibitor) [47].…”

Section: Dna Methylation and Mir-129 Expressionmentioning

confidence: 93%

“…HMGB1 can induce cell growth and migration via its intracellular signaling pathways including NF-κB, MAPK, and ERK. It has been reported that miR-129-2 could directly target HMGB1 and inhibit its expression in glioma cells [46]. Long et al exhibited a significant negative connection between expression of miR-129-5p and mobility of OS cells, suggesting a pivotal role of miR-129-5p in OS cell migration and invasion [76].…”

Section: Mir-129 and Metastasismentioning

confidence: 99%

“…MiR-129-2 was also reported to be downregulated in human glioma cancer, partially due to its DNA promoter hypermethylation. Overexpression of miR-129-2 promoted cell apoptosis at least partially through targeting the oncogene HMGB1 [46]. It was demonstrated that the apoptosis rate of cancer cells could be increased when STAT3 expression was decreased as a result of upregulation of miR-129-5p in LSCC cells [59].…”

Section: Mir-129 and Apoptosismentioning

confidence: 99%

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MicroRNA-129 in Human Cancers: from Tumorigenesis to Clinical Treatment

Gao¹,

Feng²,

Han³

et al. 2016

Cell Physiol Biochem

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Emerging evidence has shown that microRNAs (miRNAs) play essential roles in regulating human cancers development and progression. However, the underlying mechanisms remain to be further explored. MiRNAs are a class of endogenous, non-coding, 18-24 nucleotide length single-strand RNAs that moderate gene expression primarily at post-transcriptional level. There is a growing body of literature that recognizes the importance of microRNA (miR)-129 during the development of cancers. Aberrant expression of miR-129 has been detected in various types of human cancers and the validated target genes are involved in cancer-related biological processes such as DNA methylation, cell proliferation, apoptosis, cell cycle, and metastasis. In this review, we summarized the roles of miR-129 family members and their target genes in tumorigenesis and clinical treatment of human cancers, highlighting the potential roles of miR-129 as biomarkers for cancer diagnosis and prognosis, and promising tools for cancer treatment.

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Section: Mir-129 and Cell Proliferationmentioning

confidence: 66%

Section: Dna Methylation and Mir-129 Expressionmentioning

confidence: 93%

Section: Mir-129 and Metastasismentioning

confidence: 99%

Section: Mir-129 and Apoptosismentioning

confidence: 99%

See 2 more Smart Citations

MicroRNA-129 in Human Cancers: from Tumorigenesis to Clinical Treatment

Gao¹,

Feng²,

Han³

et al. 2016

Cell Physiol Biochem

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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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High‐Mobility Group Box‐1 and Liver Disease

Gaskell

Nieto

2018

Hepatology Communications

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High‐mobility group box‐1 (HMGB1) is a ubiquitous protein. While initially thought to be simply an architectural protein due to its DNA‐binding ability, evidence from the last decade suggests that HMGB1 is a key protein participating in the pathogenesis of acute liver injury and chronic liver disease. When it is passively released or actively secreted after injury, HMGB1 acts as a damage‐associated molecular pattern that communicates injury and inflammation to neighboring cells by the receptor for advanced glycation end products or toll‐like receptor 4, among others. In the setting of acute liver injury, HMGB1 participates in ischemia/reperfusion, sepsis, and drug‐induced liver injury. In the context of chronic liver disease, it has been implicated in alcoholic liver disease, liver fibrosis, nonalcoholic steatohepatitis, and hepatocellular carcinoma. Recently, specific posttranslational modifications have been identified that could condition the effects of the protein in the liver. Here, we provide a detailed review of how HMGB1 signaling participates in acute liver injury and chronic liver disease.

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MiR-129-2 functions as a tumor suppressor in glioma cells by targeting HMGB1 and is down-regulated by DNA methylation

Cited by 59 publications

References 39 publications

MicroRNA-129 in Human Cancers: from Tumorigenesis to Clinical Treatment

MicroRNA-129 in Human Cancers: from Tumorigenesis to Clinical Treatment

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

High‐Mobility Group Box‐1 and Liver Disease

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