FBP1 Is an Interacting Partner of Menin

Zaman, Shadia; Sukhodolets, Karen E.; Wang, Patricia; Qin, Jun; Levens, David; Agarwal, Sunita K.; Marx, Stephen J.

doi:10.1155/2014/535401

Cited by 5 publications

(2 citation statements)

References 29 publications

(47 reference statements)

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“…Menin has been suggested to interact with MYC and the SKI-interacting protein (SKIP) co-activator at the HIV-1 promoter (Bres, et al 2009). In HEK293 embryonic kidney cells, menin and the mixed-lineage leukemia (MLL) complex were found to interact with the transcription factor FUSE binding protein 1 (FBP1/FUSBP1) to stimulate MYC expression (Zaman, et al 2014). It was recently reported, that in fibrosarcoma cells menin can also interact directly with MYC and regulate MYC target genes in an H3K4me3-independent manner (Wu, et al 2017).…”

Section: Menin Binds To Transcription Factorsmentioning

confidence: 99%

Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1

Dreijerink¹,

Timmers²,

Brown³

2017

Endocrine-Related Cancer

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Since the discovery of the multiple endocrine neoplasia type 1 (MEN1) gene in 1997, elucidation of the molecular function of its protein product, menin, has been a challenge. Biochemical, proteomics, genetics and genomics approaches have identified various potential roles, which converge on gene expression regulation. The most consistent findings show that menin connects transcription factors and chromatin modifying enzymes, in particular the histone H3K4 methyltransferase complexes MLL1 and MLL2. Chromatin immunoprecipitation combined with next generation sequencing has enabled studying genome-wide dynamics of chromatin binding by menin. We propose that menin regulates cell type-specific transcriptional programs by linking chromatin regulatory complexes to specific transcription factors. In this fashion, the MEN1 gene is a tumor suppressor gene in the endocrine tissues that are affected in MEN1. Recent studies have hinted at possibilities to pharmacologically restore the epigenetic changes caused by loss of menin function as therapeutic strategies for MEN1, for example by inhibition of histone demethylases. The current lack of appropriate cellular model systems for MEN1-associated tumors is a limitation for compound testing, which needs to be addressed in the near future. In this review, we look back at the past twenty years of research on menin and the mechanism of disease of MEN1. In addition, we discuss how the current understanding of the molecular function of menin offers future directions to develop novel treatments for MEN1-associated endocrine tumors.

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Section: Menin Binds To Transcription Factorsmentioning

confidence: 99%

Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1

Dreijerink¹,

Timmers²,

Brown³

2017

Endocrine-Related Cancer

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“…The most recent report shows that menin can directly interact with the transactivation domain (TAD) of cMyc, and that they in turn bind to E boxes to enhance the transcription of cMyc target genes [155]. Interestingly, menin can interact with the cMyc promoter to regulate its transcription in HEK293 cells [156].…”

Section: Transcription Factorsmentioning

confidence: 99%

Involvement of the MEN1 Gene in Hormone-Related Cancers: Clues from Molecular Studies, Mouse Models, and Patient Investigations

Ziki¹,

Luo²,

Vlaeminck-Guillem³

et al. 2020

Endocrines

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MEN1 mutation predisposes patients to multiple endocrine neoplasia type 1 (MEN1), a genetic syndrome associated with the predominant co-occurrence of endocrine tumors. Intriguingly, recent evidence has suggested that MEN1 could also be involved in the development of breast and prostate cancers, two major hormone-related cancers. The first clues as to its possible role arose from the identification of the physical and functional interactions between the menin protein, encoded by MEN1, and estrogen receptor α and androgen receptor. In parallel, our team observed that aged heterozygous Men1 mutant mice developed cancerous lesions in mammary glands of female and in the prostate of male mutant mice at low frequencies, in addition to endocrine tumors. Finally, observations made both in MEN1 patients and in sporadic breast and prostate cancers further confirmed the role played by menin in these two cancers. In this review, we present the currently available data concerning the complex and multifaceted involvement of MEN1 in these two types of hormone-dependent cancers.

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Epigenetic alterations in human parathyroid tumors

et al. 2015

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Epigenetics alterations are involved in tumorigenesis and have been identified in endocrine neoplasia. In particular, DNA methylation, microRNAs deregulations and histone methylation impairment are detected in tumors of the parathyroid glands. Parathyroid tumors are the second most common endocrine neoplasia following thyroid cancer in women, and it is associated with primary hyperparathyroidism, a disease sustained by PTH hypersecretion. Despite the hallmark of global promoter hypomethylations was not detectable in parathyroid tumors, increase of hypermethylation in specific CpG islands was detected in the progression from benign to malignant parathyroid tumors. Furthermore, deregulation of a panel of embryonic-related microRNAs (miRNAs) was documented in parathyroid tumors compared with normal glands. Impaired expression of the histone methyltransferases EZH2, BMI1, and RIZ1 have been described in parathyroid tumors. Moreover, histone methyltransferases have been shown to be modulated by the oncosuppressors HIC1, MEN1, and HRPT2/CDC73 gene products that characterize tumorigenesis of parathyroid adenomas and carcinomas, respectively. The epigenetic scenario in parathyroid tumors have just began to be decoded but emerging data highlight the involvement of an embryonic gene signature in parathyroid tumor development.

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FBP1 Is an Interacting Partner of Menin

Cited by 5 publications

References 29 publications

Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1

Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1

Involvement of the MEN1 Gene in Hormone-Related Cancers: Clues from Molecular Studies, Mouse Models, and Patient Investigations

Epigenetic alterations in human parathyroid tumors

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