BDNF promotes the growth of human neurons through crosstalk with the Wnt/β-catenin signaling pathway via GSK-3β

Yang, Jinwei; Jin, Ran; Ma, Wei; Gao, Yan; Liang, Zhen; Liu, Jia; Guo, Jun; Li, Liyan

doi:10.1016/j.npep.2015.08.005

Cited by 54 publications

(30 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Based on the molecular level, Wnt/β-catenin signaling can up-regulate many kinds of cell cycle-related regulators, involving cyclin D1 and cyclin E, and down-regulate cell cycle-related inhibitors, like p21 and p27 11. Furthermore, current studies suggest that Wnt/β-catenin signaling pathway forms cross-talk with the EGF pathway, indicating the potential signaling pathway clinically involved in glioma 12. On the other hand, EGFs and EGFRs play an important role in the development of tumors by regulating cell proliferation, migration, differentiation, morphogenesis, and angiogenesis 13–15.…”

Section: Introductionmentioning

confidence: 76%

The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma

Wang

et al. 2017

OTT

View full text Add to dashboard Cite

To date, β-catenin has been reported to be implicated in mediating the epithelial-mesenchymal transition (EMT) in a variety of human cancers, which can be triggered by EGF. However, the mechanisms underlying EGF-β-catenin pathway-induced EMT of glioblastoma multiforme (GBM) have not been reported previously. In the present study, immunohistochemistry, reverse transcription polymerase chain reaction, and Western blot were applied to investigate the effect of EGF-β-catenin pathway on EMT of GBM. Here, we identified that β-catenin mRNA and protein levels were up-regulated in GBM tissues and four kinds of glioblastoma cell lines, including T98G, A172, U87, and U251 cells, compared with normal brain tissue and astrocytes. In U87 cell line, inhibition of β-catenin by siRNA suppressed EGF-induced proliferation, migration, invasiveness, and the expression of EMT activators (Snail and Slug). In addition, the expression of epithelial markers (E-cadherin) was up-regulated and the expression of mesenchymal markers (N-cadherin and MMP9) was down-regulated. Finally, inhibitor of PI3K/Akt signaling pathways inactivated the EGF-β-catenin-induced EMT. In conclusion, β-catenin-EMT pathway induced by EGF is important for GBM progression by the PI3K/Akt pathways. Inhibition of β-catenin leads to suppression of EGF pathway-induced EMT, which provides a new way to treat GBM patients.

show abstract

Section: Introductionmentioning

confidence: 76%

The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma

Wang

et al. 2017

OTT

View full text Add to dashboard Cite

show abstract

“…GSK-3 stimulates the release of interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor alpha in activated microglia and inhibits the release of anti-inflammatory cytokines like interleukin 10 (IL-10) [205]. Exercise may activate some extracellular signals that are known to inhibit GSK-3, including BDNF [180,206]. It is also possible that, as a result of a prolonged exercise, which increases the synthesis of trophic factors, there is no proinflammatory proliferation and activation of glial cells.…”

Section: Possible Mechanisms Underlying the Protective Effect Of Bndfmentioning

confidence: 99%

BDNF as a Promising Therapeutic Agent in Parkinson’s Disease

Pałasz

Wysocka

Gąsiorowska

et al. 2020

IJMS

321

197

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF) promotes neuroprotection and neuroregeneration. In animal models of Parkinson's disease (PD), BDNF enhances the survival of dopaminergic neurons, improves dopaminergic neurotransmission and motor performance. Pharmacological therapies of PD are symptom-targeting, and their effectiveness decreases with the progression of the disease; therefore, new therapeutical approaches are needed. Since, in both PD patients and animal PD models, decreased level of BDNF was found in the nigrostriatal pathway, it has been hypothesized that BDNF may serve as a therapeutic agent. Direct delivery of exogenous BDNF into the patient's brain did not relieve the symptoms of disease, nor did attempts to enhance BDNF expression with gene therapy. Physical training was neuroprotective in animal models of PD. This effect is mediated, at least partly, by BDNF. Animal studies revealed that physical activity increases BDNF and tropomyosin receptor kinase B (TrkB) expression, leading to inhibition of neurodegeneration through induction of transcription factors and expression of genes related to neuronal proliferation, survival, and inflammatory response. This review focuses on the evidence that increasing BDNF level due to gene modulation or physical exercise has a neuroprotective effect and could be considered as adjunctive therapy in PD.

show abstract

“…This survival increasing effect of exogen BDNF is temporary and dependent on functional trkB receptors (39,40). For example, within 4-5 weeks following the damage, 95% of the neurons had died although the treatment continues.…”

Section: Basic Effects Of Neurotrophinsmentioning

confidence: 99%

The role of growth factors in nerve regeneration

Önger

Delibaş

Türkmen

et al. 2016

DD&T

View full text Add to dashboard Cite

BDNF promotes the growth of human neurons through crosstalk with the Wnt/β-catenin signaling pathway via GSK-3β

Cited by 54 publications

References 73 publications

The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma

The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma

BDNF as a Promising Therapeutic Agent in Parkinson’s Disease

The role of growth factors in nerve regeneration

Contact Info

Product

Resources

About

BDNF promotes the growth of human neurons through crosstalk with the Wnt/β-catenin signaling pathway via GSK-3β

Cited by 54 publications

References 73 publications

The critical role of EGF-&beta;-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma

The critical role of EGF-&beta;-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma

BDNF as a Promising Therapeutic Agent in Parkinson’s Disease

The role of growth factors in nerve regeneration

Contact Info

Product

Resources

About

The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma

The critical role of EGF-β-catenin signaling in the epithelial-mesenchymal transition in human glioblastoma