E-Cadherin Expression Distinguishes Mouse from Human Hematopoiesis in the Basophil and Erythroid Lineages

Krimpenfort, Rosa A.; Behr, Felix M.; Nieuwland, Marja; Rink, Iris de; Kerkhoven, Ron; Lindern, Marieke von; Nethe, Micha

doi:10.3390/biom12111706

Cited by 2 publications

(2 citation statements)

References 68 publications

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“…The link between E-cadherin and hematopoiesis has been demonstrated in erythroid progenitors and it has been shown that E-cadherin has an erythroid lineage-restricted expression in BM cells and is involved in the maturation of erythroid progenitors [78]. Consistent with this, it was shown that E-cadherin is predominantly expressed in the basophil/mast cell lineage in mouse BM and that inhibition of E-cadherin causes a disruption of erythroid differentiation [78][79][80]. However, E-cadherin does not seem to be expressed in human basophils [79].…”

Section: E-cadherin In Acute Leukemiamentioning

confidence: 72%

“…Consistent with this, it was shown that E-cadherin is predominantly expressed in the basophil/mast cell lineage in mouse BM and that inhibition of E-cadherin causes a disruption of erythroid differentiation [78][79][80]. However, E-cadherin does not seem to be expressed in human basophils [79]. Although it is not easy to explain this phenomenon based on the existing literature, it can be envisioned as being a result of the evolutionary process.…”

Section: E-cadherin In Acute Leukemiamentioning

confidence: 84%

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Epithelial–Mesenchymal Transition in Acute Leukemias

Varisli,

Vlahopoulos

2024

IJMS

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Epithelial–mesenchymal transition (EMT) is a metabolic process that confers phenotypic flexibility to cells and the ability to adapt to new functions. This transition is critical during embryogenesis and is required for the differentiation of many tissues and organs. EMT can also be induced in advanced-stage cancers, leading to further malignant behavior and chemotherapy resistance, resulting in an unfavorable prognosis for patients. Although EMT was long considered and studied only in solid tumors, it has been shown to be involved in the pathogenesis of hematological malignancies, including acute leukemias. Indeed, there is increasing evidence that EMT promotes the progression of acute leukemias, leading to the emergence of a more aggressive phenotype of the disease, and also causes chemotherapy resistance. The current literature suggests that the levels and activities of EMT inducers and markers can be used to predict prognosis, and that targeting EMT in addition to conventional therapies may increase treatment success in acute leukemias.

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Section: E-cadherin In Acute Leukemiamentioning

confidence: 72%

Section: E-cadherin In Acute Leukemiamentioning

confidence: 84%

Epithelial–Mesenchymal Transition in Acute Leukemias

Varisli,

Vlahopoulos

2024

IJMS

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E-cadherin/β-catenin expression is conserved in human and rat erythropoiesis and marks stress erythropoiesis

Krimpenfort,

van der Meulen,

Verhagen

et al. 2023

Blood Advances

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E-cadherin is a crucial regulator of epithelial cell-cell adhesion and an established tumor suppressor. Aside epithelia, E-cadherin expression marks the erythroid cell lineage during human, but not mouse hematopoiesis. However, the role of E-cadherin in human erythropoiesis remains unknown. Because rat erythropoiesis was postulated to reflect human erythropoiesis more closely then mouse erythropoiesis, we investigated E-cadherin expression in rat erythroid progenitors. E-cadherin expression is conserved within the erythroid lineage between rat and human. In response to anemia, erythroblasts in rat bone marrow (BM) upregulate E-cadherin, as well as its binding partner β-catenin. CRISPR/Cas9-mediated knock out of E-cadherin, revealed that E-cadherin expression is required to stabilize β-catenin in human and rat erythroblasts. Suppression of β-catenin degradation by GSK3β inhibitor CHIR99021 also enhances β-catenin stability in human erythroblasts, but hampers erythroblast differentiation and survival. In contrast, direct activation of β-catenin signaling, using an inducible, stable β-catenin variant, does not perturb maturation or survival of human erythroblasts but rather enhances their differentiation. Whereas human erythroblasts do not respond to WNT ligands and direct GSK3β inhibition even reduces their survival, we postulate that β-catenin stability and signaling is mostly controlled by E-cadherin in human and rat erythroblasts. In response to anemia, E-cadherin driven upregulation and subsequent activation of β-catenin signaling may stimulate erythroblast differentiation to support stress erythropoiesis in BM. Overall, we uncover E-cadherin/β-catenin expression to mark stress erythropoiesis in rat BM. This may provide further understanding of the underlying molecular regulation of stress erythropoiesis in BM, which is currently poorly understood.

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E-Cadherin Expression Distinguishes Mouse from Human Hematopoiesis in the Basophil and Erythroid Lineages

Cited by 2 publications

References 68 publications

Epithelial–Mesenchymal Transition in Acute Leukemias

Epithelial–Mesenchymal Transition in Acute Leukemias

E-cadherin/β-catenin expression is conserved in human and rat erythropoiesis and marks stress erythropoiesis

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