Jagged1/Notch3 Signaling Modulates Hemangioma-Derived Pericyte Proliferation and Maturation

Ji, Yi; Chen, Siyuan; Xiang, Bo; Li, Yuan; Li, Li; Wang, Qi

doi:10.1159/000453148

Cited by 24 publications

(18 citation statements)

References 39 publications

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“…The role of the Notch pathway in cancers has been determined according to the effect of Notch pathway on cell proliferation, migration, and invasion [22][23][24][25][26]. In the present study, we demonstrated that TRIM67 overexpression can upregulate Notch1, Jagged1, and NICD.…”

Section: Discussionsupporting

confidence: 58%

TRIM67 Promotes the Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Positively Regulating the Notch Pathway

Jiang¹,

Ren²,

Xu³

et al. 2020

J. Cancer

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Tripartite motif-containing 67 (TRIM67), an E3 ubiquitin ligase, belongs to the TRIM protein family. The relationship between TRIM67 and tumorigenesis is not fully clear. Here, we elucidated TRIM67 function in non-small cell lung cancer (NSCLC). TRIM67 immunostaining results were correlated with clinicopathological features. Moreover, the function of TRIM67 in cultured NSCLC cells was evaluated by MTT, colony formation, and Transwell assays. TRIM67 expression was associated with tumor size, lymph node metastasis, p-TNM stage, cancer cell differentiation, and poor prognosis. We altered TRIM67 expression in A549 and H1299 cell lines, and the results showed that TRIM67 promoted cell proliferation, migration, invasion and EMT by positively regulating the Notch pathway. Collectively, the results showed that TRIM67 promotes NSCLC progression through the Notch pathway and that TRIM67 expression is associated with clinicopathological features, indicating that TRIM67 may play an important role in promoting the development of NSCLC and could be applied as not only an important prognostic biomarker but also a therapeutic target in NSCLC.

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Section: Discussionsupporting

confidence: 58%

TRIM67 Promotes the Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Positively Regulating the Notch Pathway

Jiang¹,

Ren²,

Xu³

et al. 2020

J. Cancer

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“…This multipotency is analogous to cells belonging to the heterogeneous multipotent stromal population previously referred to as "mesenchymal stem cells" but more commonly described now as "mesenchymal progenitors." In fact, cultured pericytes display broader multipotency compared to mesenchymal progenitors, including differentiation into vascular smooth muscle cells, myofibroblasts as well as parenchymal cells such as skeletal and cardiac myocytes and neuronal cells (Barron et al, 2016;Ji et al, 2016;Birbrair et al, 2017;Siedlecki et al, 2018;Alarcon-Martinez et al, 2019). The broad multipotency reported for pericytes is the basis on which some researchers postulate that pericytes are the predominant source of tissue resident mesenchymal progenitors (Crisan et al, 2008;da Silva Meirelles et al, 2008).…”

Section: Activation Multipotency and Fate Specificity Of Pericytesmentioning

confidence: 99%

“…Besides the regulation imposed by cell adhesion molecules, pericyte quiescence is promoted by Notch signaling. Notch3 on pericytes interacts directly with Jagged-1 on endothelial cells to promote pericyte-endothelial cell adhesion while also inhibiting pericyte proliferation and migration (Liu et al, 2009(Liu et al, , 2010Schulz et al, 2015;Ji et al, 2016). Notch signaling is implicated in the regulation of quiescence and metabolism in many cell types (Iso et al, 2003;Liu et al, 2010;Koch et al, 2013), through diverse actions that include downregulated expression of glycolytic enzymes such as PFKFB3 (De Bock et al, 2013;Bayin et al, 2017).…”

Section: Quiescencementioning

confidence: 99%

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Metabolic Coordination of Pericyte Phenotypes: Therapeutic Implications

Nwadozi

Rudnicki

Haas

2020

Front. Cell Dev. Biol.

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Pericytes are mural vascular cells found predominantly on the abluminal wall of capillaries, where they contribute to the maintenance of capillary structural integrity and vascular permeability. Generally quiescent cells in the adult, pericyte activation and proliferation occur during both physiological and pathological vascular and tissue remodeling. A considerable body of research indicates that pericytes possess attributes of a multipotent adult stem cell, as they are capable of self-renewal as well as commitment and differentiation into multiple lineages. However, pericytes also display phenotypic heterogeneity and recent studies indicate that lineage potential differs between pericyte subpopulations. While numerous microenvironmental cues and cell signaling pathways are known to regulate pericyte functions, the roles that metabolic pathways play in pericyte quiescence, self-renewal or differentiation have been given limited consideration to date. This review will summarize existing data regarding pericyte metabolism and will discuss the coupling of signal pathways to shifts in metabolic pathway preferences that ultimately regulate pericyte quiescence, self-renewal and trans-differentiation. The association between dysregulated metabolic processes and development of pericyte pathologies will be highlighted. Despite ongoing debate regarding pericyte classification and their functional capacity for trans-differentiation in vivo, pericytes are increasingly exploited as a cell therapy tool to promote tissue healing and regeneration. Ultimately, the efficacy of therapeutic approaches hinges on the capacity to effectively control/optimize the fate of the implanted pericytes. Thus, we will identify knowledge gaps that need to be addressed to more effectively harness the opportunity for therapeutic manipulation of pericytes to control pathological outcomes in tissue remodeling.

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“…Furthermore, some results indicated that Notch-3 inhibition could help enhance the sensitivity to paclitaxel [ 38 , 39 ]. Recent findings have suggested that the Notch pathway is one of the most important signal pathways in tumor development or progression [ 40 ]. Overall, other results also have proved that Notch-3 protein significantly affects the development and prognosis of lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Effect of Notch-3-Specific Inhibition and Paclitaxel in Non-Small Cell Lung Cancer (NSCLC) Cells Via Activation of The Intrinsic Apoptosis Pathway

Jiao

et al. 2017

Med Sci Monit

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BackgroundLung cancers are resistant to conventional chemotherapeutic interventions such as paclitaxel. Notch signaling is crucial in the chemoresistance of lung cancer cells. The Notch inhibitor gamma-secretase inhibitor (GSI) inhibits the Notch signaling pathway.Material/MethodsHere, we evaluated how Notch-3 inhibition by GSI can enhance the sensitivity of lung cancer cells to paclitaxel. To study how Notch-3-specific inhibition affects non-small cell lung cancer (NSCLC), we compared the cell viability, apoptosis, and colony formation of A549 and H1299 cells treated with Notch-3 siRNA and GSI.ResultsThe expression levels of Notch-3 or Notch intracellular domain 3 (NICD3) and apoptosis-related proteins were measured and compared between different groups. Notch-3 was significantly overexpressed in both cell lines, and Notch-3 expression was elevated after paclitaxel treatment, indicating activation of the Notch signaling pathway. Inhibition of the Notch signaling pathway by GSI and Notch-3 siRNA reduced cell proliferation and induced apoptosis in A549 and H1299 cells, thereby boosting sensitivity of the cell lines to paclitaxel. Concomitant treatment with paclitaxel and GSI or siRNA downregulated Bcl-2 expression and upregulated Bax expression levels.ConclusionsThese results indicate a synergistic effect of Notch-3-specific inhibition and paclitaxel through alteration of the intrinsic apoptosis pathway, which was involved in Notch-3-induced chemoresistance in NSCLC cells, and GSI inhibited Notch-3-induced chemoresistance in a concentration-dependent manner. This approach that combines Notch-3-specific inhibition and paclitaxel would be likely to apply in NSCLC.

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Jagged1/Notch3 Signaling Modulates Hemangioma-Derived Pericyte Proliferation and Maturation

Cited by 24 publications

References 39 publications

TRIM67 Promotes the Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Positively Regulating the Notch Pathway

TRIM67 Promotes the Proliferation, Migration, and Invasion of Non-Small-Cell Lung Cancer by Positively Regulating the Notch Pathway

Metabolic Coordination of Pericyte Phenotypes: Therapeutic Implications

Synergistic Effect of Notch-3-Specific Inhibition and Paclitaxel in Non-Small Cell Lung Cancer (NSCLC) Cells Via Activation of The Intrinsic Apoptosis Pathway

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