Down-regulation of the Lamin A/C in neuroblastoma triggers the expansion of tumor initiating cells

Nardella, Marta; Guglielmi, Loredana; Musa, Carla; Iannetti, Ilaria; Maresca, Giovanna; Amendola, Donatella; Porru, Manuela; Carico, Elisabetta; Sessa, Giuseppe; Camerlingo, Rosa; Dominici, Carlo; Megiorni, Francesca; Milan, Marika; Bearzi, Claudia; Rizzi, Roberto; Pirozzi, Giuseppe; Leonetti, Carlo; Bucci, Barbara; Mercanti, Delio; Felsani, Armando; D’Agnano, Igea

doi:10.18632/oncotarget.5104

Cited by 24 publications

(25 citation statements)

References 44 publications

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“…These pathways are already implicated in stem cell phenotypes in cancer, but studies have yet to address the potential involvement of lamin A/C in the CSC phenotype promoted by these signalling events. Nonetheless, Nardella et al (2015) demonstrated that depletion of A-type lamins in a neuroblastoma cell line resulted in a cell subpopulation with enhanced stem cell characteristics. The authors suggest that this phenotype was mediated by altered expression of microRNA-101, which results in upregulation of the MYC proto-oncogene, and reveals an inverse correlation between expression of lamin A/C and MYC in human neuroblastoma biopsies (Nardella et al, 2015).…”

Section: Lamin A/c and Cancer Stem Cellsmentioning

confidence: 99%

“…Nonetheless, Nardella et al (2015) demonstrated that depletion of A-type lamins in a neuroblastoma cell line resulted in a cell subpopulation with enhanced stem cell characteristics. The authors suggest that this phenotype was mediated by altered expression of microRNA-101, which results in upregulation of the MYC proto-oncogene, and reveals an inverse correlation between expression of lamin A/C and MYC in human neuroblastoma biopsies (Nardella et al, 2015). Based on our emerging understanding of lamins and their role in stemness and differentiation, the decreased levels of lamin A/C in human cancers may both reflect and promote CSC qualities for proliferation and differentiation, which can determine tumour growth, metastasis, and response to therapeutics.…”

Section: Lamin A/c and Cancer Stem Cellsmentioning

confidence: 99%

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Causes and consequences of nuclear envelope alterations in tumour progression

Bell

Lammerding

2016

European Journal of Cell Biology

112

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Morphological changes in the size and shape of the nucleus are highly prevalent in cancer, but the underlying molecular mechanisms and the functional relevance remain poorly understood. Nuclear envelope proteins, which can modulate nuclear shape and organization, have emerged as key components in a variety of signalling pathways long implicated in tumourigenesis and metastasis. The expression of nuclear envelope proteins is altered in many cancers, and changes in levels of nuclear envelope proteins lamins A and C are associated with poor prognosis in multiple human cancers. In this review we highlight the role of the nuclear envelope in different processes important for tumour initiation and cancer progression, with a focus on lamins A and C. Lamin A/C controls many cellular processes with key roles in cancer, including cell invasion, stemness, genomic stability, signal transduction, transcriptional regulation, and resistance to mechanical stress. In addition, we discuss potential mechanisms mediating the changes in lamin levels observed in many cancers. A better understanding of cause-and-effect relationships between lamin expression and tumour progression could reveal important mechanisms for coordinated regulation of oncogenic processes, and indicate therapeutic vulnerabilities that could be exploited for improved patient outcome.

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Section: Lamin A/c and Cancer Stem Cellsmentioning

confidence: 99%

Section: Lamin A/c and Cancer Stem Cellsmentioning

confidence: 99%

Causes and consequences of nuclear envelope alterations in tumour progression

Bell

Lammerding

2016

European Journal of Cell Biology

112

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“…Selective silencing of lamin A/C triggers the formation of NB-iCSCs with self-renewing ability. Loss of lamin A/C is also MYCN expression-dependent [150] . SOX2, a member of the SRY-related high mobility group box, is a transcription factor that is mostly expressed during embryonic development.…”

Section: Induced Cscs and Therapy Resistancementioning

confidence: 98%

“…For instance, Lamin A/C, the type V intermediate filaments of nuclear lamina, is often reduced or absent in proliferative cells of various tumors [148,149] . Lack of lamin A/C predisposes cells towards an immature phenotype and influences the presence of tumor-initiating cells in NB [150] . Selective silencing of lamin A/C triggers the formation of NB-iCSCs with self-renewing ability.…”

Section: Induced Cscs and Therapy Resistancementioning

confidence: 99%

Cancer stem cells in neuroblastoma therapy resistance

Aravindan¹,

Jain²,

Somasundaram³

et al. 2019

CDR

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Neuroblastoma (NB) is the most common cancer of infancy and accounts for nearly one tenth of pediatric cancer deaths. This mortality rate has been attributed to the > 50% frequency of relapse despite intensive, multimodal clinical therapy in patients with progressive NB. Given the disease's heterogeneity and developed resistance, attaining a cure after relapse of progressive NB is highly challenging. A rapid decrease in the timeline between successive recurrences is likely due to the ongoing acquisition of genetic rearrangements in undifferentiated NB-cancer stem cells (CSCs). In this review, we present the current understanding of NB-CSCs, their intrinsic role in tumorigenesis, their function in disease progression, and their influence on acquired therapy resistance and tumor evolution. In particular, this review focus on the intrinsic involvement of stem cells and signaling in the genesis of NB, the function of pre-existing CSCs in NB progression and therapy response, the formation and influence of induced CSCs (iCSCs) in drug resistance and tumor evolution, and the development of a CSC-targeted therapeutic approach.

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“…In neuroblastoma cell lines, miR-101 and one of its targets, LaminA, may control neuroblastoma stem-like cell self-renewal and tumor-propagating properties. 13 Therefore, neuroblastoma stem-like cells meet criteria for stem-like or progenitor cells (multilineage differentiation) and tumor-initiating cells, and ongoing efforts are aimed at ablating these cells, and/or forcing their differentiation.…”

Section: Neuroblastoma As An Aberration Of Neural Crest Developmentmentioning

confidence: 99%

The “neuro” of neuroblastoma: Neuroblastoma as a neurodevelopmental disorder

Ratner

Brodeur

Dale

et al. 2016

Annals of Neurology

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Neuroblastoma is a childhood cancer derived from cells of neural crest origin. The hallmarks of its enigmatic character include its propensity for spontaneous regression under some circumstances and its association with paraneoplastic opsoclonus, myoclonus, and ataxia. The neurodevelopmental underpinnings of its origins may provide important clues for development of novel therapeutic and preventive agents for this frequently fatal malignancy and for the associated paraneoplastic syndromes.

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Down-regulation of the Lamin A/C in neuroblastoma triggers the expansion of tumor initiating cells

Cited by 24 publications

References 44 publications

Causes and consequences of nuclear envelope alterations in tumour progression

Causes and consequences of nuclear envelope alterations in tumour progression

Cancer stem cells in neuroblastoma therapy resistance

The “neuro” of neuroblastoma: Neuroblastoma as a neurodevelopmental disorder

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