Invasion of white matter tracts by glioma stem cells is regulated by a NOTCH1–SOX2 positive-feedback loop

Wang, Jun; Xu, Senlin; Duan, Jiang‐Jie; Lv, Yi; Guo, Yufeng; Shi, Yu; Li, Lin; Yang, Zeyu; Liao, Xuemei; Cai, Jiao; Zhang, Yanqi; Xiao, Hualiang; Li, Yin; Wu, Hao; Zhang, Jingna; Lv, Sheng‐Qing; Yang, Qingkai; Yang, Xiaojun; Jiang, Tao; Zhang, Xia; Bian, Xiu‐Wu; Yu, Shanshan

doi:10.1038/s41593-018-0285-z

Cited by 138 publications

(101 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, SP1 binds to the MDK gene promoter and directly promotes MDK expression, showing the SP1‐MDK axis cooperated in glioma tumourigenesis . More and more lncRNAs have been identified to participate in the gliomagenesis with increasing evidence, such as, lncRNA FOXD2‐AS1 is up‐regulated in glioma tissue/cells and CCND2 is also up‐regulated. Then, the up‐regulation of CCND2 was closely correlated with poor prognosis of glioma patients and CCND2 knockdown suppresses the cellular proliferation, migration, invasion and EMT in glioma cells via miR‐185‐5p and FOXD2‐AS1 regulation .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR‐124‐3p/CCND2 axis

Liu

Yang

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Mounting evidence suggests the vital roles of long noncoding RNA (lncRNAs) in the glioma. However, the role of LINC00511 in gliomagenesis is still uncovered. Here, in this study, we aim to investigate the effects of LINC00511 on the glioma cancer phenotype and its deepgoing mechanism. Results indicated that LINC00511 was up‐regulated in glioma tissues and cell lines, moreover its overexpression positively correlated with the poor prognosis and advanced pathological stages. For the upstream regulation, LINC00511 was epigenetically up‐regulated by transcription factor specificity protein 1 (SP1). Gain and loss of functional experiments demonstrated that LINC00511 promoted the proliferation and invasion of glioma cells in vitro. The knockdown of LINC00511 repressed the tumour growth in vivo. Mechanistically, LINC00511 positively regulated the CCND2 expression via competitively sponging with miR‐124‐3p. Overall, our finding illuminates that LINC00511 is induced by SP1 and accelerates the glioma progression through targeting miR‐124‐3p/CCND2 axis, constructing the SP1/LINC00511/miR‐124‐3p/CCND2 axis.

show abstract

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR‐124‐3p/CCND2 axis

Liu

Yang

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Neural precursor cells in the SVZ provide chemoattractant and proinvasive signals to DIPG cells through secretion of pleiotrophin, which maintains RhoA and ROCK signaling (Qin et al 2017). Jagged, a NOTCH ligand expressed along axons, supports GSC invasion along unmyelinated white matter tracts through up-regulating SOX9 and SOX2 in GSCs (Wang et al 2019). Furthermore, GSCs adapt to conditions outside of their typical environmental niche.…”

Section: Gsc Microenvironment: Essential Niche Factorsmentioning

confidence: 99%

Glioblastoma stem cells: lessons from the tumor hierarchy in a lethal cancer

et al. 2019

View full text Add to dashboard Cite

Glioblastoma ranks among the most lethal of all human cancers. Glioblastomas display striking cellular heterogeneity, with stem-like glioblastoma stem cells (GSCs) at the apex. Although the original identification of GSCs dates back more than a decade, the purification and characterization of GSCs remains challenging. Despite these challenges, the evidence that GSCs play important roles in tumor growth and response to therapy has grown. Like normal stem cells, GSCs are functionally defined and distinguished from their differentiated tumor progeny at core transcriptional, epigenetic, and metabolic regulatory levels, suggesting that no single therapeutic modality will be universally effective against a heterogenous GSC population. Glioblastomas induce a systemic immunosuppression with mixed responses to oncoimmunologic modalities, suggesting the potential for augmentation of response with a deeper consideration of GSCs. Unfortunately, the GSC literature has been complicated by frequent use of inferior cell lines and a lack of proper functional analyses. Collectively, glioblastoma offers a reliable cancer to study cancer stem cells to better model the human disease and inform improved biologic understanding and design of novel therapeutics.

show abstract

“…Interestingly, NOTCH signaling is also augmented in hypoxic tumor regions by Vasorin-mediated stabilization of NICD, and hypoxia-induced expression of Vasorin promotes glioma aggressiveness [ 130 ]. Finally, there is evidence for dormant GSC populations residing at the invasive front of the tumor [ 131 ], where Jagged1 expressed by nerve fibers could facilitate NOTCH1 + CD133 + glioma cell invasion of white matter tracts through a SOX9-SOX2-NOTCH1 feedback loop [ 132 ].…”

Section: Notch As An Oncogene In Gliomamentioning

confidence: 99%

Oncogenic and Tumor-Suppressive Functions of NOTCH Signaling in Glioma

Parmigiani

Taylor

Giachino

2020

Cells

View full text Add to dashboard Cite

Although the role of NOTCH signaling has been extensively studied in health and disease, many questions still remain unresolved. Being crucial for tissue homeostasis, NOTCH signaling is also implicated in multiple cancers by either promoting or suppressing tumor development. In this review we illustrate the context-dependent role of NOTCH signaling during tumorigenesis with a particular focus on gliomas, the most frequent and aggressive brain tumors in adults. For a long time, NOTCH has been considered an oncogene in glioma mainly by virtue of its neural stem cell-promoting activity. However, the recent identification of NOTCH-inactivating mutations in some glioma patients has challenged this notion, prompting a re-examination of the function of NOTCH in brain tumor subtypes. We discuss recent findings that might help to reconcile the controversial role of NOTCH signaling in this disease, and pose outstanding questions that still remain to be addressed.

show abstract

Invasion of white matter tracts by glioma stem cells is regulated by a NOTCH1–SOX2 positive-feedback loop

Cited by 138 publications

References 45 publications

Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR‐124‐3p/CCND2 axis

Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR‐124‐3p/CCND2 axis

Glioblastoma stem cells: lessons from the tumor hierarchy in a lethal cancer

Oncogenic and Tumor-Suppressive Functions of NOTCH Signaling in Glioma

Contact Info

Product

Resources

About