Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator

Duan, Wei; Zhang, Yuping; Hou, Zhi; Huang, Chen; Zhu, He; Zhang, Chunqing; Yin, Qian

doi:10.1007/s12035-015-9122-5

Cited by 201 publications

(153 citation statements)

References 100 publications

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“…3a,b). NEUN is a marker of mature neurons2021; however, consistent with previous observations222324, distribution of NEUN immunofluorescence was heterogeneous in the SCN, with stronger expression in a central region and minimal expression in dorsal and medial regions (Fig. 3a,b).…”

Section: Resultssupporting

confidence: 90%

Persistent neuronal Ube3a expression in the suprachiasmatic nucleus of Angelman syndrome model mice

Jones

Han

DeBruyne

et al. 2016

Sci Rep

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Mutations or deletions of the maternal allele of the UBE3A gene cause Angelman syndrome (AS), a severe neurodevelopmental disorder. The paternal UBE3A/Ube3a allele becomes epigenetically silenced in most neurons during postnatal development in humans and mice; hence, loss of the maternal allele largely eliminates neuronal expression of UBE3A protein. However, recent studies suggest that paternal Ube3a may escape silencing in certain neuron populations, allowing for persistent expression of paternal UBE3A protein. Here we extend evidence in AS model mice (Ube3am–/p+) of paternal UBE3A expression within the suprachiasmatic nucleus (SCN), the master circadian pacemaker. Paternal UBE3A-positive cells in the SCN show partial colocalization with the neuropeptide arginine vasopressin (AVP) and clock proteins (PER2 and BMAL1), supporting that paternal UBE3A expression in the SCN is often of neuronal origin. Paternal UBE3A also partially colocalizes with a marker of neural progenitors, SOX2, implying that relaxed or incomplete imprinting of paternal Ube3a reflects an overall immature molecular phenotype. Our findings highlight the complexity of Ube3a imprinting in the brain and illuminate a subpopulation of SCN neurons as a focal point for future studies aimed at understanding the mechanisms of Ube3a imprinting.

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Section: Resultssupporting

confidence: 90%

Persistent neuronal Ube3a expression in the suprachiasmatic nucleus of Angelman syndrome model mice

Jones

Han

DeBruyne

et al. 2016

Sci Rep

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“…Positive staining for NeuN suggests the neuronal nature of neoplasms and is considered to be a reliable marker for clear cell neoplasms of the central nervous system, which include CN, oligodendroglioma, and clear cell ependymoma [48889]. It has also been reported that positive staining for NeuN correlates with a lower proliferation index [490].…”

Section: Histopathological Analysis and Molecular Pathogenesismentioning

confidence: 99%

Central Neurocytoma: A Review of Clinical Management and Histopathologic Features

Lee

Bui

Chen

et al. 2016

Brain Tumor Res Treat

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Central neurocytoma (CN) is a rare, benign brain tumor often located in the lateral ventricles. CN may cause obstructive hydrocephalus and manifest as signs of increased intracranial pressure. The goal of treatment for CN is a gross total resection (GTR), which often yields excellent prognosis with a very high rate of tumor control and survival. Adjuvant radiosurgery and radiotherapy may be considered to improve tumor control when GTR cannot be achieved. Chemotherapy is also not considered a primary treatment, but has been used as a salvage therapy. The radiological features of CN are indistinguishable from those of other brain tumors; therefore, many histological markers, such as synaptophysin, can be very useful for diagnosing CNs. Furthermore, the MIB-1 Labeling Index seems to be correlated with the prognosis of CN. We also discuss oncogenes associated with these elusive tumors. Further studies may improve our ability to accurately diagnose CNs and to design the optimal treatment regimens for patients with CNs.

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“…In human, RBFOX3 is a protein-coding gene located on chromosome 17 and comprised of 15 exons [14]. As the third member of the RNA-binding fox family of proteins, RBFOX3 plays a role in alternative pre-mRNA splicing via binding to the conserved UGCAUG element in the upstream intron [15].…”

Section: Introductionmentioning

confidence: 99%

RBFOX3 Regulates the Chemosensitivity of Cancer Cells to 5-Fluorouracil via the PI3K/AKT, EMT and Cytochrome-C/Caspase Pathways

Liu¹,

Wu²,

Li³

et al. 2018

Cell Physiol Biochem

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Background/Aims: RBFOX3, an RNA-binding fox protein, plays an important role in the differentiation of neuronal development, but its role in the chemosensitivity of hepatocellular carcinoma (HCC) to 5-FU is unknown. Methods: In this study, we examined the biological functions of RBFOX3 and its effect on the chemosensitivity of HCC cells to 5-FU in vitro and in a mouse xenograft model. Results: RBFOX3 was found to have elevated expression in HCC cell lines and tissue samples, and its knockdown inhibited HCC cell proliferation. Moreover, knockdown of RBFOX3 improved the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and enhanced the apoptosis induced by 5-FU. However, overexpression of RBFOX3 reduced the inhibitory effect of 5-fluorouracil (5-FU) on cell proliferation, migration and invasion, and decreased the apoptosis induced by 5-FU. We further elucidated that RBFOX3 knockdown synergized with 5-FU to inhibit the growth and invasion of HCC cells through PI3K/AKT and epithelial-mesenchymal transition (EMT) signaling, and promote apoptosis by activating the cytochrome-c/caspase signaling pathway. Finally, we validated that RBFOX3 regulated 5-FU-mediated cytotoxicity in HCC in mouse xenograft models. Conclusions: The findings from this study indicate that RBFOX3 regulates the chemosensitivity of HCC to 5-FU in vitro and in vivo. Therefore, targeting RBFOX3 may improve the inhibition of HCC growth and progression by 5-FU, and provide a novel potential therapeutic strategy for HCC.

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Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator

Cited by 201 publications

References 100 publications

Persistent neuronal Ube3a expression in the suprachiasmatic nucleus of Angelman syndrome model mice

Persistent neuronal Ube3a expression in the suprachiasmatic nucleus of Angelman syndrome model mice

Central Neurocytoma: A Review of Clinical Management and Histopathologic Features

RBFOX3 Regulates the Chemosensitivity of Cancer Cells to 5-Fluorouracil via the PI3K/AKT, EMT and Cytochrome-C/Caspase Pathways

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