Cell Biology Meets Cell Metabolism: Energy Production Is Similar in Stem Cells and in Cancer Stem Cells in Brain and Bone Marrow

Noorden, C. J. F. Van; Breznik, Barbara; Novak, Metka; Dijck, Amber J van; Tanan, Saloua; Vittori, Miloš; Bogataj, Urban; Bakker, Noëlle; Khoury, Joseph D.; Molenaar, Remco J.; Hira, Vashendriya V.V.

doi:10.1369/00221554211054585

Cited by 9 publications

(29 citation statements)

References 243 publications

(388 reference statements)

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“…In order to explain the lipid metabolism-associated metabolic switch, it has been speculated that proliferating NSCs activate lipogenesis in order to increase the amount of lipids available, that will later be use for plasma membrane synthesis (Knobloch, 2017). On the other hand, quiescent (non-proliferative) NSC use fatty acid oxidation to cover their energetic demands and maintain their stemness (van Noorden et al, 2022).…”

Section: Metabolic Requirements Of the Neural Stem Cell Nichementioning

confidence: 99%

Metabolic regulation of the neural stem cell fate: Unraveling new connections, establishing new concepts

et al. 2022

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The neural stem cell niche is a key regulator participating in the maintenance, regeneration, and repair of the brain. Within the niche neural stem cells (NSC) generate new neurons throughout life, which is important for tissue homeostasis and brain function. NSCs are regulated by intrinsic and extrinsic factors with cellular metabolism being lately recognized as one of the most important ones, with evidence suggesting that it may serve as a common signal integrator to ensure mammalian brain homeostasis. The aim of this review is to summarize recent insights into how metabolism affects NSC fate decisions in adult neural stem cell niches, with occasional referencing of embryonic neural stem cells when it is deemed necessary. Specifically, we will highlight the implication of mitochondria as crucial regulators of NSC fate decisions and the relationship between metabolism and ependymal cells. The link between primary cilia dysfunction in the region of hypothalamus and metabolic diseases will be examined as well. Lastly, the involvement of metabolic pathways in ependymal cell ciliogenesis and physiology regulation will be discussed.

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Section: Metabolic Requirements Of the Neural Stem Cell Nichementioning

confidence: 99%

Metabolic regulation of the neural stem cell fate: Unraveling new connections, establishing new concepts

et al. 2022

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“…[ 33 ] Our study revealed that compared to adherent cells, BCSCs have a higher FAO level, which is consistent with the fact that CSCs primarily rely on FAO‐mediated metabolic processes. [ 27,54 ] In addition, our data show that CD96 interacts with Src and facilitates phosphorylation of Stat3 in BCSCs, linking this interaction with the regulation of FAO in these cells. These results suggest that CD96‐Src regulates FAO in BCSCs via the Stat3 pathway.…”

Section: Discussionmentioning

confidence: 65%

Tumor Cell‐Intrinsic CD96 Mediates Chemoresistance and Cancer Stemness by Regulating Mitochondrial Fatty Acid β‐Oxidation

Xia

et al. 2022

Advanced Science

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Targeting CD96 that originates in immune cells has shown potential for cancer therapy. However, the role of intrinsic CD96 in solid tumor cells remains unknown. Here, it is found that CD96 is frequently expressed in tumor cells from clinical breast cancer samples and is correlated with poor long‐term prognosis in these patients. The CD96+ cancer cell subpopulations exhibit features of both breast cancer stem cells and chemoresistance. In vivo inhibition of cancer cell‐intrinsic CD96 enhances the chemotherapeutic response in a patient‐derived tumor xenograft model. Mechanistically, CD96 enhances mitochondrial fatty acid β‐oxidation via the CD155‐CD96‐Src‐Stat3‐Opa1 pathway, which subsequently promotes chemoresistance in breast cancer stem cells. A previously unknown role is identified for tumor cell‐intrinsic CD96 and an attractive target in improving the chemotherapeutic response.

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“…The results demonstrated that modulation of PCAT‐1 influences the activity of PKM2, which subsequently affects the levels of β‐catenin, factor that is vital in the regulation of osteogenic differentiation 33 . In particular, MSCs that were subjected to vector PCAT‐1 treatment exhibited reduced concentrations of total β‐catenin 34 . This observation implies that PCAT‐1 regulates osteogenic differentiation by activating PKM2 and inhibiting the activities of β‐catenin.…”

Section: Discussionmentioning

confidence: 87%

PCAT‐1′ s role in wound healing impairment: Mitochondrial dysfunction and bone marrow stem cell differentiation inhibition via PKM2/β‐catenin pathway and its impact on implant osseo‐integration

Deng,

Liu,

et al. 2023

International Wound Journal

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This study focused on unravelling the role of PCAT‐1 in wound‐healing process, particularly its impact on regenerative and osteogenic abilities of mesenchymal stem cells (MSCs). We delved into how PCAT‐1 regulates mitochondrial oxidative phosphorylation (OXPHOS) and interacts with pivotal molecular pathways, especially β‐catenin and PKM2, using human bone marrow‐derived MSCs. MSCs were cultured under specific conditions and PCAT‐1 expression was modified through transfection. We thoroughly assessed several critical parameters: MSC proliferation, mitochondrial functionality, ATP production and expression of wound healing and osteogenic differentiation markers. Further, we evaluated alkaline phosphatase (ALP) activity and mineral deposition, essential for bone healing. Our findings revealed that overexpressing PCAT‐1 significantly reduced MSC proliferation, hampered mitochondrial performance and lowered ATP levels, suggesting the clear inhibitory effect of PCAT‐1 on these vital wound‐healing processes. Additionally, PCAT‐1 overexpression notably decreased ALP activity and calcium accumulation in MSCs, crucial for effective bone regeneration. This overexpression also led to the reduction in osteogenic marker expression, indicating suppression of osteogenic differentiation, essential in wound‐healing scenarios. Moreover, our study uncovered a direct interaction between PCAT‐1 and the PKM2/β‐catenin pathway, where PCAT‐1 overexpression intensified PKM2 activity while inhibiting β‐catenin, thereby adversely affecting osteogenesis. This research thus highlights PCAT‐1's significant role in impairing wound healing, offering insights into the molecular mechanisms that may guide future therapeutic strategies for enhancing wound repair and bone regeneration.

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Cell Biology Meets Cell Metabolism: Energy Production Is Similar in Stem Cells and in Cancer Stem Cells in Brain and Bone Marrow

Cited by 9 publications

References 243 publications

Metabolic regulation of the neural stem cell fate: Unraveling new connections, establishing new concepts

Metabolic regulation of the neural stem cell fate: Unraveling new connections, establishing new concepts

Tumor Cell‐Intrinsic CD96 Mediates Chemoresistance and Cancer Stemness by Regulating Mitochondrial Fatty Acid β‐Oxidation

PCAT‐1′ s role in wound healing impairment: Mitochondrial dysfunction and bone marrow stem cell differentiation inhibition via PKM2/β‐catenin pathway and its impact on implant osseo‐integration

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