The microRNA-212/132 cluster regulates B cell development by targeting Sox4

Mehta, Arnav; Mann, Mati; Zhao, Jimmy L.; Marinov, Georgi K.; Majumdar, Devdoot; Garcia-Flores, Yvette; Du, Xiaomi; Erikçi, Erdem; Chowdhury, Kamal; Baltimore, David

doi:10.1083/jcb.2107oia191

Cited by 13 publications

(15 citation statements)

References 43 publications

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“…Furthermore, the cluster was also found to be involved in altering lymphoid cell differentiation via the transcription factor PU.1 (37). An increasing number of studies demonstrated that several miRNA clusters may regulate the occurrence and development of cancer by cooperating with the c-Myc oncogene (38)(39)(40). The association of miR-23a/24-2/27a with c-Myc has also been investigated and the findings suggested that the miR-23a/24-2/27a cluster was upregulated in breast cancer and was correlated with cancer cell metastasis, migration and invasion via c-Myc (34).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑23a/24‑2/27a as a potential diagnostic biomarker for cancer: A systematic review and meta‑analysis

et al. 2017

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Abstract. An increasing number of studies have proven that microRNAs play an important role in the occurrence, development and prognosis of various types of cancer. As a vital gene cluster, the microRNA (miR)-23a/24-2/27a cluster may be an important marker for predicting cancer prognosis and tumor progression. A search was conducted through PubMed, Medline and the Cochrane Library to identify studies investigating the association between the miR-23a/24-2/27a cluster and cancer, and the identified related studies were included in the present meta-analysis. The strength of the association was assessed by hazard ratio (HR) and its 95% confidence interval (95% CI). A total of 21 studies were included in this meta-analysis. The results indicated that a high level of miR-23a exerted a significant effect on overall survival (OS) (HR=2.33, 95% CI: 1.18-4.58; P=0.014), but not on disease-free survival (DFS)/recurrence-free survival (RFS) (HR=1.13, 95% CI: 0.37-3.44; P=0.836). There was an obvious statistically significant association between OS and the expression of miR-24 (HR=2.49, 95% CI: 1.84-3.37; P=0.000), particularly in the digestive system (pooled HR=2.99, 95% CI: 2.17-4.13, P=0.000). In addition, the result suggested a statistically significant association between the expression of miR-27a and OS (pooled HR=1.89, 95% CI: 1.32-2.69; P=0.001), as well as DFS/RFS/progression-free survival (HR=2.19, 95% CI: 1.29-3.70; P=0.003), particularly in renal cell carcinoma (HR=2.30, 95% CI: 1.16-4.67; P=0.017). A subgroup analysis by ethnicity, cancer type and statistical methodology was performed. There was no obvious publication bias. In conclusion, the present study demonstrated that the miR-23a/24-2/27a cluster may be a useful marker for predicting cancer prognosis and tumor progression. IntroductionMicroRNAs (miRNAs, miRs) are ~22-nucleotide long, single-stranded non-coding RNA molecules (1). They were first discovered in the nematode Caenorhabditis elegans with the identification of the developmental regulator lin-4 (2). Thus far, there are ~2,588 annotated miRNAs found in the human genome (3). With advances in research, it has been demonstrated that miRNAs may play an important role in various diseases. An increasing number of miRNAs were proven to participate in crucial biological processes, such as cell proliferation, migration, invasion and apoptosis (4-7), which may enable use of the miRNA family in the diagnosis and treatment of disease, due to the extensive alterations in miRNA expression in different diseases.miR-23a/24-2/27a encodes a ~2,159-nt pri-miRNA transcript, which is located in chromosome 19p13.12 as an intergenic miRNA cluster (8). The profiling analysis suggested that the miR-23a/24-2/27a cluster was significantly upregulated in hepatocellular carcinoma (HCC) (9), pancreatic adenocarcinoma (10) and breast cancer (11). There are several studies on the association of the miR-23a/24-2/27a cluster with various types of cancer. Thus, the present systematic review and meta-analysis were designed to confirm...

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑23a/24‑2/27a as a potential diagnostic biomarker for cancer: A systematic review and meta‑analysis

et al. 2017

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“…In several preclinical cancer models, miR-212 shows the ability to suppress solid tumor growth 6 8. It has been documented that miR-212 is involved in B-cell development9 and interleukin-17-producing T helper cell differentiation 10. Most interestingly, miR-212 overexpression can inhibit B-cell cancer development induced by oncogenes such as c-Myc 9.…”

Section: Introductionmentioning

confidence: 99%

“…It has been documented that miR-212 is involved in B-cell development9 and interleukin-17-producing T helper cell differentiation 10. Most interestingly, miR-212 overexpression can inhibit B-cell cancer development induced by oncogenes such as c-Myc 9. However, the link between miR-212 expression and T-cell lymphoma development is still elusive.…”

Section: Introductionmentioning

confidence: 99%

Restoration of microRNA-212 Causes a G0/G1 Cell Cycle Arrest and Apoptosis in Adult T-Cell Leukemia/Lymphoma Cells by Repressing CCND3 Expression

Wang

Guo

Yang

et al. 2017

Journal of Investigative Medicine

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Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive T-cell malignancy. This study was designed to explore the expression and functional significance of microRNA (miR)-212 in ATL. The expression of miR-212 in human ATL tissues and cell lines were investigated. Gain-of-function experiments were carried out to determine the roles of miR-212 in cell proliferation, tumorigenesis, cell cycle progression, and apoptosis. We also identified and functionally characterized the target genes of miR-212 in ATL cells. Compared with normal lymph node biopsies, lymphoma samples from ATL patients displayed underexpression of miR-212 (p=0.0032). Consistently, miR-212 was downregulated in human ATL cell lines, compared with normal T lymphocytes. Restoration of miR-212 significantly (p<0.05) inhibited ATL cell proliferation and tumorigenesis in mice. Overexpression of miR-212 led to an accumulation of G0/G1-phase cells and a concomitant reduction of S-phase cells. Moreover, enforced expression of miR-212-induced significant apoptosis in ATL cells. CCND3, which encodes a cell cycle regulator cyclin D3, was identified as a direct target of miR-212 in ATL cells. Rescue experiments with a miR-212-resistant variant of CCND3 demonstrated that overexpression of CCND3 restored cell-cycle progression and attenuated apoptotic response in miR-212-overexpressing ATL cells. Taken together, miR-212 exerts growth-suppressive effects in ATL cells largely by targeting CCND3 and may have therapeutic potential in ATL.

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“…during the early development of B cells in bone marrow is highly expressed mir-181a (ref. 126 ), but alleviated levels of mir-132 are required for early transition of pro-B cells 127 . similarly, the over-expressed mir-17-92 cluster is essential for survival of B cell precursors, differentiation from pro-B to pre-B cells and latter into immature B cells 128,129 , however, there are variations between adult and paediatric age 129 .…”

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MicroRNAs in the key events of systemic lupus erythematosus pathogenesis

Hušáková¹

2016

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. Small non-coding RNA molecules (miRs) are involved in immune cell maturation and function and might influence immunopathological processes of systemic lupus erythematosus (SLE) pathogenesis. Methods and Results. This paper presents the results of a literature search for publications dealing with the relationship between miRs and pathological factors related to SLE such as genetic background, immune dysregulation and gender-associated differences participating in SLE development. In SLE, distinct miRs are differentially expressed in SLE cells of innate and adaptive immunity. The miR-146a and miR-155 genes, among others, interfere with intracellular signalling pathways downstream of toll-like receptors 7 and 9 (TLR-7, TLR-9) and influences interferon (IFN)-type I synthesis in plasmacytoid dendritic cells. In T and B cells, miR-126, miR-21, miR-146a, miR-155, miR-1246 and others might influence gene expression by epigenetic modifications, support abnormal cytosine release, differentiation of cell subsets, B cell hyperactivity and autoantibody production. Besides, estrogen might up-and downregulate immunologically active miRs, which are potential mediators of hormonal influences in SLE development. Moreover, SLE genetic basis included some polymorphisms of the miR-146a gene, which varies across populations. Conclusion. Distinct miRs are differentially expressed in both SLE mice models and human patients and promote autoimmune features of immune processes. MiRs are important molecules modulating susceptibility to SLE as well as its onset, clinical diversity and progression.

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The microRNA-212/132 cluster regulates B cell development by targeting Sox4

Cited by 13 publications

References 43 publications

MicroRNA‑23a/24‑2/27a as a potential diagnostic biomarker for cancer: A systematic review and meta‑analysis

MicroRNA‑23a/24‑2/27a as a potential diagnostic biomarker for cancer: A systematic review and meta‑analysis

Restoration of microRNA-212 Causes a G0/G1 Cell Cycle Arrest and Apoptosis in Adult T-Cell Leukemia/Lymphoma Cells by Repressing CCND3 Expression

MicroRNAs in the key events of systemic lupus erythematosus pathogenesis

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