TPT1 Supports Proliferation of Neural Stem/Progenitor Cells and Brain Tumor Initiating Cells Regulated by Macrophage Migration Inhibitory Factor (MIF)

Morimoto, Yukina; Tokumitsu, Ayako; Sone, Takefumi; Hirota, Yuki; Tamura, Ryota; Sakamoto, Ayuna; Nakajima, Kazunori; Toda, Masahiro; Kawakami, Yutaka; Ohta, Shigeki

doi:10.1007/s11064-022-03629-6

Cited by 7 publications

(2 citation statements)

References 37 publications

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“…Table 2). In contrast, the genes that had enhanced expression in Beclin1-null cells were cell stress, metabolism, and neurodevelopment genes, such as Tpt1 59 , Tmxb4x 60 , Snapin 61 , Nptn 62 , Tcf4 63 , and Cplx2 64 (Fig 6B). Additionally, Beclin1-null cells showed upregulation in cell stress-related transcripts such as reactive oxygen species genes (ROS; e.g., Romo1 65 , Pet100 66 , Ndufa3 67 ; Suppl.…”

Section: Resultsmentioning

confidence: 99%

Mitotic Activity and DNA Maintenance of Adult Neural Stem Cells is Regulated by Beclin1

Kalinina,

Dhaliwal,

Xue

et al. 2024

Preprint

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Beclin1 is a tumor suppressor gene that can regulate proliferation under pathological conditions. Whether Beclin1 has a role in regulating proliferation in physiological conditions remains unknown. Here, through the creation of an inducible transgenic mouse that removes Beclin1 from adult neural stem and progenitor cells (NSPCs) and their progeny we uncovered that Beclin1 is required cell-autonomously to sustain proliferating NSCPs in vivo and ex vivo. Flow cytometry analysis and single-cell RNA-sequencing show that Beclin1 is required for mitosis. Additional analysis of the proliferating NSPCs resolved by stage of cell cycle uncovered that Beclin1-null cells have a distinct differential developmental trajectory accompanied by downregulation of genes involved in chromosomal maintenance and upregulation of cell stress genes upon cell cycle exit. These effects align with DNA damage in Beclin1-null cells and ultimately result in less adult-born granular neurons. Together these data identify Beclin1 as a novel regulator of mitosis in adult NSPCs.

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Section: Resultsmentioning

confidence: 99%

Mitotic Activity and DNA Maintenance of Adult Neural Stem Cells is Regulated by Beclin1

Kalinina,

Dhaliwal,

Xue

et al. 2024

Preprint

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“…PTPRZ1 receptor and pleiotrophin (PTN) growth factor interaction promotes glioblastoma migration and invasion and promote neural stem cells (NSCs) signalling for glioma invasion to the subventricular zone (Lu et al, 2005; Qin et al, 2017; Zhang et al, 2021). Meanwhile, TPT1 has been shown to interact with macrophage migratory inhibitory factor (MIF) to promote the proliferation and maintenance of these NSCs, and their migration to the ventricular zone (Morimoto et al, 2022). PTN and MIF were identified as key signaling factors from the CellChat analysis, and PTN was also identified as a transition gene by MuTrans.…”

Section: Discussionmentioning

confidence: 99%

Cell fate dynamics reconstruction identifies TPT1 and PTPRZ1 feedback loops as master regulators of differentiation in pediatric glioblastoma-immune cell networks

Uthamacumaran

2023

Preprint

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Pediatric glioblastoma is a complex dynamical disease that is difficult to treat due to its multiple adaptive behaviors driven largely by phenotypic plasticity. Integrated data science and network theory pipelines offer novel approaches to study glioblastoma cell fate dynamics, particularly phenotypic transitions over time. Here we used various single-cell trajectory inference algorithms to infer signaling dynamics regulating pediatric glioblastoma-immune cell networks. We identified GATA2, PTPRZ1, TPT1, MTRNR2L1/2, OLIG1/2, SOX11, PDGFRA, EGFR, S100B, WNT, TNFα, and NF-kB as critical transition genes or signals regulating glioblastoma-immune network dynamics, revealing potential clinically relevant targets. Further, we reconstructed glioblastoma cell fate attractors and found complex bifurcation dynamics within glioblastoma phenotypic transitions, suggesting that a causal pattern may be driving glioblastoma evolution and cell fate decision-making. Together, our findings have implications for the development of targeted therapies against glioblastoma, and the continued integration of quantitative approaches to understand pediatric glioblastoma tumour-immune interactions.

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Cell Fate Dynamics Reconstruction Identifies TPT1 and PTPRZ1 Feedback Loops as Master Regulators of Differentiation in Pediatric Glioblastoma-Immune Cell Networks

Uthamacumaran

2024

Interdiscip Sci Comput Life Sci

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TPT1 Supports Proliferation of Neural Stem/Progenitor Cells and Brain Tumor Initiating Cells Regulated by Macrophage Migration Inhibitory Factor (MIF)

Cited by 7 publications

References 37 publications

Mitotic Activity and DNA Maintenance of Adult Neural Stem Cells is Regulated by Beclin1

Mitotic Activity and DNA Maintenance of Adult Neural Stem Cells is Regulated by Beclin1

Cell fate dynamics reconstruction identifies TPT1 and PTPRZ1 feedback loops as master regulators of differentiation in pediatric glioblastoma-immune cell networks

Cell Fate Dynamics Reconstruction Identifies TPT1 and PTPRZ1 Feedback Loops as Master Regulators of Differentiation in Pediatric Glioblastoma-Immune Cell Networks

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