MAP3K11 is a tumor suppressor targeted by the oncomiR miR-125b in early B cells

Knackmuss, U; Lindner, Silke E.; Aneichyk, Tatsiana; Kotkamp, Bianka; Knust, Z; Villunger, Andreas; Herzog, Sebastian

doi:10.1038/cdd.2015.87

Cited by 28 publications

(27 citation statements)

References 56 publications

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“…The pre-B cell lines 1676 and 74 have already been described [23,62]. The pre-B cell lines 1676 and 74 have already been described [23,62].…”

Section: Cells Cell Culture and Retroviral Transductionmentioning

confidence: 99%

“…For the 3 0 -UTR assay, UTRs of interest were cloned by PCR and ligated into LMP-destGFP [62] 3 0 of the destabilized GFP cDNA via XhoI and ClaI. In short, overlapping forward and reverse PCR primers were designed based on the mature miRNA sequence, for example, CAAGACCTGTgatTCTACCTTCCGT and atcACAGGTCTTGACGGA AGGTAGA (lower cases mark the mismatch region, the linker between the binding sites in underlined) for miR-1839 (AAGGTAG ATAGAACAGGTCTTG).…”

Section: Plasmid Constructsmentioning

confidence: 99%

“…The pre-B cell lines wk3, 1587, and 1677 were derived by extended culture of total bone marrow of SLP-65 À/À and SLP-65 À/À LAT À/À mice, respectively, in IL-7-supplemented medium. The pre-B cell lines 1676 and 74 have already been described [23,62]. Pre-B cells were cultured in IMDM (Sigma) containing 7.5% FCS (Biochrom Superior), 100 U/ml penicillin, 100 U/ml streptomycin (PAN), and 50 lM 2-ME.…”

Section: Cells Cell Culture and Retroviral Transductionmentioning

confidence: 99%

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The miR‐15 family reinforces the transition from proliferation to differentiation in pre‐B cells

et al. 2017

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Precursor B lymphocytes expand upon expression of a pre-B cell receptor (pre-BCR), but then transit into a resting state in which immunoglobulin light chain gene recombination is initiated. This bi-phasic sequence is orchestrated by the IL-7 receptor (IL-7R) and pre-BCR signaling, respectively, but little is known about microRNAs fine-tuning these events. Here, we show that pre-B cells lacking miR-15 family functions exhibit prolonged proliferation due to aberrant expression of the target genes cyclin E1 and D3. As a consequence, they fail to trigger the transcriptional reprogramming normally accompanying their differentiation, resulting in a developmental block at the pre-B cell stage. Intriguingly, our data indicate that the miR-15 family is suppressed by both IL-7R and pre-BCR signaling, suggesting it is actively integrated into the regulatory circuits of developing B cells. These findings identify the miR-15 family as a novel element required to promote the switch from pre-B cell proliferation to differentiation.

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“…The pre-B cell lines 1676 and 74 have already been described [23,62]. The pre-B cell lines 1676 and 74 have already been described [23,62].…”

Section: Cells Cell Culture and Retroviral Transductionmentioning

confidence: 99%

Section: Plasmid Constructsmentioning

confidence: 99%

Section: Cells Cell Culture and Retroviral Transductionmentioning

confidence: 99%

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The miR‐15 family reinforces the transition from proliferation to differentiation in pre‐B cells

et al. 2017

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“…These findings might be compatible with our data of PVR gene body methylation perhaps leading to gene transcription promotion in KA and SCC. On the other hand, Knackmuss et al reported that MAP3K11 protein might function as an important tumor suppressor neutralized by oncomiR-125b in B-cell leukemia [24], although the function of MAP3K11 in epidermal tumors is unknown.…”

Section: Discussionmentioning

confidence: 99%

Aberrant DNA Methylation in Keratoacanthoma

Nobeyama

Nakagawa

2016

PLoS ONE

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BackgroundKeratoacanthoma (KA) is a self-limiting epidermal tumor for which histopathological examination sometimes suggests malignancy. Based on inconsistent clinical views, KA can be regarded as both a benign tumor and a variant of squamous cell carcinoma (SCC). Aberrant DNA methylation frequently occurs in malignant tumors but it scarcely occurs in benign tumors. Whether aberrant methylation occurs in KA has not been previously examined.ObjectiveThe aim is to elucidate whether aberrant methylation of CpG islands (CGI) containing a high density of cytosine-guanine dinucleotide (CpG) sites occurs in KA.MethodsFive SCC cell lines, two cultured samples of normal human epidermal keratinocytes (NHEKs), 18 clinical SCC samples, and 21 clinical KA samples were analyzed with Infinium HumanMethylation450 BeadChips, quantitative real-time methylation-specific PCR (RT-MSP) and/or bisulfite sequencing.ResultsGenome-wide analyses of NHEK, KA, and SCC indicated that there was a greater number of aberrantly hypermethylated CGIs in SCC than in KA and there were aberrantly hypermethylated CGIs which are common in both. Among the common hypermethylated CGIs, RT-MSP and bisulfite sequencing targeting CGIs located on CCDC17, PVR, and MAP3K11 gene bodies also showed that methylation levels were significantly higher in KA than in normal epidermis. Statistical analyses suggested that the methylation level of CGI located on PVR in SCC might be correlated to lymph node metastasis (P = 0.013, Mann-Whitney U test) and that the methylation level of CGI in MAP3K11 in KA might be correlated to age (P = 0.031, linear regression analysis).ConclusionAberrant DNA methylation occurs in KA.

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“…[7][8][9][10][11] Several target genes have been identified and postulated to have a role in the oncogenic properties of overexpressed miR-125b, such as Trp53inp1 and MAP3K11, which facilitate cell survival. 8,12 A genetic deletion of the gene encoding IRF4 has also been reported in miR-125b dysregulationinduced B cells. 11 In addition to promoting leukemia, several in vitro studies also suggest a role for this microRNA in B-cell development and differentiation.…”

Section: Introductionmentioning

confidence: 99%