Pro-oncogenic Roles of HLXB9 Protein in Insulinoma Cells through Interaction with Nono Protein and Down-regulation of the c-Met Inhibitor Cblb (Casitas B-lineage Lymphoma b)

Desai, Shruti; Kharade, Sampada S.; Parekh, Vaishali I.; Iyer, Sucharitha; Agarwal, Sunita K.

doi:10.1074/jbc.m115.661413

Cited by 10 publications

(16 citation statements)

References 42 publications

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“…In this regard, MNX1 expression is known to be regulated by Menin, the protein product of MEN1 . Though it has been reported that loss of Menin function increases MNX1 expression [32]], and MNX1 has also been shown to function as an oncogene in driving pancreatic islet cell tumorigenesis [44][45] [46], we did not observe substantial expression of MNX1 in any of our tumors.…”

Section: Men1 Mutation and Copy Number Losscontrasting

confidence: 64%

Temporal and Clonal Progression in a Pediatric Ependymoma Patient Through Multiple Treatments

Miller

Dahiya²,

Li³

et al. 2017

Preprint

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Section: Men1 Mutation and Copy Number Losscontrasting

confidence: 64%

Temporal and Clonal Progression in a Pediatric Ependymoma Patient Through Multiple Treatments

Miller

Dahiya²,

Li³

et al. 2017

Preprint

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“…Cell culture, stable cell lines, and inhibitor treatments. Mouse MIN6-4N insulinoma cells (56)(57)(58) were maintained in low-glucose Dulbecco modified Eagle medium (DMEM) supplemented with 15% fetal bovine serum (FBS) and antibiotic/antimycotic (Thermo Fisher Scientific, Waltham, MA) at 37°C and 5% CO 2 . Vec-4N (here referred to as V6-1) and M27-4N (here referred to as Men1) are stable MIN6 lines containing the vector pcDNA3.1-Myc-His or pcDNA3.1-Myc-His-menin, respectively (7).…”

Section: Methodsmentioning

confidence: 99%

Long Noncoding RNA MEG3 Is an Epigenetic Determinant of Oncogenic Signaling in Functional Pancreatic Neuroendocrine Tumor Cells

Iyer

Modali

Agarwal

2017

Molecular and Cellular Biology

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The long noncoding RNA (lncRNA) MEG3 is significantly downregulated in pancreatic neuroendocrine tumors (PNETs). MEG3 loss corresponds with aberrant upregulation of the oncogenic hepatocyte growth factor (HGF) receptor c-MET in PNETs. Meg3 overexpression in a mouse insulin-secreting PNET cell line, MIN6, downregulates c-Met expression. However, the molecular mechanism by which MEG3 regulates c-MET is not known. Using romatinsolation by NAurification and uencing (ChIRP-Seq), we identified Meg3 binding to unique genomic regions in and around the c-Met gene. In the absence of Meg3, these c-Met regions displayed distinctive enhancer-signature histone modifications. Furthermore, Meg3 relied on functional enhancer of zeste homolog 2 (EZH2), a component of polycomb repressive complex 2 (PRC2), to inhibit c-Met expression. Another mechanism of lncRNA-mediated regulation of gene expression utilized triplex-forming GA-GT rich sequences. Transfection of such motifs from Meg3 RNA, termed triplex-forming oligonucleotides (TFOs), in MIN6 cells suppressed c-Met expression and enhanced cell proliferation, perhaps by modulating other targets. This study comprehensively establishes epigenetic mechanisms underlying Meg3 control of c-Met and the oncogenic consequences of Meg3 loss or c-Met gain. These findings have clinical relevance for targeting c-MET in PNETs. There is also the potential for pancreatic islet β-cell expansion through c-MET regulation to ameliorate β-cell loss in diabetes.

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“… 3 , 9 , 10 , 11 Furthermore, it has been demonstrated to be oncogenic in prostate cancer and insulinoma. 12 , 13 …”

Section: Introductionmentioning

confidence: 99%

Expression, Clinical Significance, and Functional Prediction of MNX1 in Breast Cancer

Tian

Wang

Zhu

et al. 2018

Molecular Therapy - Nucleic Acids

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Motor neuron and pancreas homeobox 1 (MNX1) is a key developmental gene. Previous studies found that it was upregulated in several tumors, but its role in breast cancer (BC) remains unclear. In order to have a better understanding of this gene in BC, we examined the expression of MNX1 in BC tissues and normal breast tissues by qRT-PCR and by analyzing data from The Cancer Genome Atlas (TCGA) database. We also assessed the association of MNX1 expression with BC clinicopathological features and investigated the impact of MNX1 on BC survival. Potential molecular function of MNX1 was predicted through protein-protein interactions and functional enrichment. The results showed that the expression of MNX1 was significantly increased in BC tissues, especially in the HER2-positive subtype, and MNX1 expression was associated with several clinical characteristics, including menopause status, receptor status, subtypes, tumor size, lymph node metastasis, and race. In addition, patients with higher MNX1 expression had poorer survival. Enrichment analysis suggested that MNX1 is probably involved in biological processes and pathways related to nuclear division, cell cycle, and p53 signaling. In conclusion, our study suggests that MNX1 may act as a tumor promoter in BC. We hope these findings will draw more attention to MNX1 in future cancer studies.

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Pro-oncogenic Roles of HLXB9 Protein in Insulinoma Cells through Interaction with Nono Protein and Down-regulation of the c-Met Inhibitor Cblb (Casitas B-lineage Lymphoma b)

Cited by 10 publications

References 42 publications

Temporal and Clonal Progression in a Pediatric Ependymoma Patient Through Multiple Treatments

Temporal and Clonal Progression in a Pediatric Ependymoma Patient Through Multiple Treatments

Long Noncoding RNA MEG3 Is an Epigenetic Determinant of Oncogenic Signaling in Functional Pancreatic Neuroendocrine Tumor Cells

Expression, Clinical Significance, and Functional Prediction of MNX1 in Breast Cancer

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