BCL11A Facilitates Cell Proliferation and Metastasis in Neuroblastoma via
Regulating the PI3K/Akt Signaling Pathway

Jin, Qianya; Chen, Yanmin; Du, Shibei; Xu, Dongqing; Yue, Juanqing; Yuan, Xiaojun

doi:10.2174/1568009622666220728123748

Cited by 6 publications

(1 citation statement)

References 29 publications

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“…Alteration of the expression of BCL11A is associated with dysregulation of the hematopoietic system and progression to B cell malignancies[36]. Knockdown of BCL11A leads to quiescence, decreasing the proliferation of hematopoietic stem cells [29,37] while its overexpression is associated with the growth of some solid tumors, such as laryngeal squamous cell carcinoma and neuroblastoma [38,39]. In this study, we explored the cellular and molecular consequences of BCL11A on adult Erys in response to corticosteroids.…”

Section: Discussionmentioning

confidence: 99%

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent

Mazzarini,

Cherone,

Nguyen

et al. 2024

Preprint

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Prior evidence indicates that the erythroid cellular response to glucocorticoids (GC) has developmental specificity, namely, that developmentally more advanced cells that are undergoing or have undergone fetal to adult globin switching are more responsive to GC-induced expansion. To investigate the molecular underpinnings of this, we focused on the major developmental globin regulator BCL11A. We compared:a)levels of expression and nuclear content of BCL11A in adult erythroid cells upon GC stimulation;b)response to GC of CD34+ cells from patients withBCL11Amicrodeletions and reducedBCL11Aexpression, and;c)response to GC of two cellular models (HUDEP-2 and adult CD34+ cells) before and after reduction ofBCL11Aexpression by shRNA. We observed that:a)GC-expanded erythroid cells from a large cohort of blood donors displayed amplified expression and nuclear accumulation of BCL11A;b)CD34+ cells fromBCL11Amicrodeletion patients generated fewer erythroid cells when cultured with GC compared to their parents, while the erythroid expansion of the patients was similar to that of their parents in cultures without GC, and;c)adult CD34+ cells and HUDEP-2 cells with shRNA-depleted expression ofBCL11Aexhibit reduced expansion in response to GC. In addition, RNA-seq profiling of shRNA-BCL11A CD34+ cells cultured with and without GC was similar (very few differentially expressed genes), while GC-specific responses (differential expression ofGILZand of numerous additional genes) were observed only in controls cells with unperturbed BCL11A expression. These data indicate that BCL11A is an important participant of certain aspects of the stress pathway sustained by GC.

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Section: Discussionmentioning

confidence: 99%

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent

Mazzarini,

Cherone,

Nguyen

et al. 2024

Preprint

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RNA-seq analysis reveals candidate genes associated with proliferation, invasion, and migration in BCL11A knockdown B-NHL cell lines

et al. 2023

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Epithelial to Mesenchymal Transition in Neuroblastoma: Mechanisms and Therapeutic Considerations

Jahangiri

2024

Curr. Tissue Microenviron. Rep.

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Purpose of Review Neuroblastoma (NB) is a solid tumour of the extracranial region in children, and it originates from the developing sympathetic nervous system. Metastasis is present in circa 70% of NB cases at the time of diagnosis and may be accompanied by poor prognosis and resistance to treatment. As such, metastasis is an important step in NB progression and is the main cause of fatality in this cancer. Furthermore, metastasis is linked to epithelial to mesenchymal transition (EMT). Recent Findings EMT is characterised by the loss of the stationary compact epithelial cell arrangement and increased motility and invasion of these cells and may also be associated with patient outcomes, including treatment resistance, recurrence, and poor survival. Summary This study aims to gain mechanistic insight into EMT and review signalling pathways, proteins, non-coding RNA, and microenvironmental factors that may contribute to this process in NB. Further, drug compounds that affect EMT in NB, and proteins and non-coding RNA that impact EMT and treatment resistance will be reviewed. A better comprehension of EMT in NB will deepen our understanding of this cancer and provide new avenues for clinical interventions and therapeutic gain.

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BCL11A Facilitates Cell Proliferation and Metastasis in Neuroblastoma via Regulating the PI3K/Akt Signaling Pathway

Cited by 6 publications

References 29 publications

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent

RNA-seq analysis reveals candidate genes associated with proliferation, invasion, and migration in BCL11A knockdown B-NHL cell lines

Epithelial to Mesenchymal Transition in Neuroblastoma: Mechanisms and Therapeutic Considerations

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