The β-catenin signaling pathway induces aggressive potential in breast cancer by up-regulating the chemokine CCL5

Yasuhara, Rika; Irié, Tarou; Suzuki, Kenya; Sawada, Terumasa; Miwa, Noriko; Sasaki, Akira; Tsunoda, Yuko; Nakamura, Seigo; Mishima, Kenji

doi:10.1016/j.yexcr.2015.09.003

Cited by 30 publications

(23 citation statements)

References 48 publications

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“…6-Bio docks with GSK3B better than other inhibitors such as indirubin, hymenialdisine and meridianins 23 . It also increases the accumulation of CTNNB1/β-catenin due to the inhibition GSK3B, thus promoting aggression of breast cancer cells 24 . 6-Bio also indirectly activates canonical WNT5A signaling in the hippocampal neurons to protect them from Aβ oligomers 12 .…”

Section: Discussionmentioning

confidence: 99%

A novel autophagy modulator 6-Bio ameliorates SNCA/α-synuclein toxicity

et al. 2017

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Parkinson disease (PD) is a life-threatening neurodegenerative movement disorder with unmet therapeutic intervention. We have identified a small molecule autophagy modulator, 6-Bio that shows clearance of toxic SNCA/α-synuclein (a protein implicated in synucleopathies) aggregates in yeast and mammalian cell lines. 6-Bio induces autophagy and dramatically enhances autolysosome formation resulting in SNCA degradation. Importantly, neuroprotective function of 6-Bio as envisaged by immunohistology and behavior analyses in a preclinical model of PD where it induces autophagy in dopaminergic (DAergic) neurons of mice midbrain to clear toxic protein aggregates suggesting that it could be a potential therapeutic candidate for protein conformational disorders.

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Section: Discussionmentioning

confidence: 99%

A novel autophagy modulator 6-Bio ameliorates SNCA/α-synuclein toxicity

et al. 2017

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“…The Wnt1 gene, originally named Int-1, was identified in 1982, which was activated by integration of mouse mammary tumor virus [4]. Dysregulated expression of Wnt signaling is involved in the initiation of various tumors such as hematological malignancies and gastric, lung, pancreatic and breast tumors [5–9]. In addition to the variety of tumors, Wnt proteins are linked to many other human diseases [10].…”

Section: Discussionmentioning

confidence: 99%

Impairment of Wnt/β-catenin signaling in blood cells of patients with severe cavitary pulmonary tuberculosis

et al. 2017

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Tuberculosis (TB) remains as a leading infectious disease worldwide. Our previous study showed interferon (IFN)-γ and CD3 T cell impairment in patients with severe cavitary pulmonary TB (PTB). However, the cause of the change in immune responses during the progression of TB is still poorly understood. In this study, eight newly diagnosed patients with severe cavitary and mild lesion non-cavity PTB were recruited, and three healthy volunteers were recruited as the control. RNA extracted from blood was tested by whole genome oligo microarrays. A PCR array was used to further test the same samples. Two additional groups of patients were recruited according to the same criteria with healthy control(HC) recruited as well and subjected to peripheral blood mononuclear cell isolation (PBMC)and analysis of TCF-7, β-catenin, cyclin D2, IFN-γ, and tumor necrosis factor (TNF)-α expression in CD14- cells (lymphocytes) and CD14+ cells by quantitative PCR. The changes of expression of β-catenin, CD69+ and IFN-γ by CD3+, CD14- and CD14+ cells in vitro with stimulation of LiCl were tested by flow cytometry. Whole genome oligo microarrays showed a significant decrease in expression of the Wnt signaling pathway in severe PTB patients. Further analysis of the Wnt pathway by PCR array indicated that TCF-7, β-catenin, and cyclin D2 expression was significantly reduced in severe PTB patients compared with mild PTB patients. In the additionally recruited patients, TCF-7, β-catenin, and cyclin D2 were expressed in both CD14+ and CD14- cells, while β-catenin was decreased significantly in CD14- cells compared with CD14+ cells in severe PTB patients, and IFN-γ and TNF-α expression in CD14- cells was also reduced significantly in severe PTB patients. β-catenin can directly trigger T cell activation and IFN-γsecretion in PBMCs stimulated for 24 hours. These findings indicate that Wnt pathway and its key genes, such as β-catenin, were impaired in blood cells of patients with severe PTB. Therefore, Wnt/β-catenin pathway is closely associated with T cell proliferation and TB lesion deterioration.

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“…However, RhoA was reported to regulate chemokine expression to induce cell migration (Kim et al, ). Furthermore, β‐catenin expression enhances tumor progression via chemokine production in breast cancers (Yasuhara et al, ). Metastasis of pancreatic cancer cells is closely related to chemokine SDF‐1/CXCR4 receptor signaling that is regulated by Wnt/β‐catenin (Wang and Ma, ).…”

Section: Discussionmentioning

confidence: 99%

Wnt3A Induces GSK‐3β Phosphorylation and β‐Catenin Accumulation Through RhoA/ROCK

Kim

Choi

et al. 2016

Journal Cellular Physiology

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In canonical pathway, Wnt3A has been known to stabilize β-catenin through the dissociation between β-catenin and glycogen synthase kinase-3β (GSK-3β) that suppresses the phosphorylation and degradation of β-catenin. In non-canonical signaling pathway, Wnt was known to activate Rho GTPases and to induce cell migration. The cross-talk between canonical and non-canonical pathways by Wnt signaling; however, has not been fully elucidated. Here, we revealed that Wnt3A induces not only the phosphorylation of GSK-3β and accumulation of β-catenin but also RhoA activation in RAW264.7 and HEK293 cells. Notably, sh-RhoA and Tat-C3 abolished both the phosphorylation of GSK-3β and accumulation of β-catenin. Y27632, an inhibitor of Rho-associated coiled coil kinase (ROCK) and si-ROCK inhibited both GSK-3β phosphorylation and β-catenin accumulation. Furthermore, active domain of ROCK directly phosphorylated the purified recombinant GSK-3β in vitro. In addition, Wnt3A-induced cell proliferation and migration, which were inhibited by Tat-C3 and Y27632. Taken together, we propose the cross-talk between canonical and non-canonical signaling pathways of Wnt3A, which induces GSK-3β phosphorylation and β-catenin accumulation through RhoA and ROCK activation. J. Cell. Physiol. 232: 1104-1113, 2017. © 2016 Wiley Periodicals, Inc.

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The β-catenin signaling pathway induces aggressive potential in breast cancer by up-regulating the chemokine CCL5

Cited by 30 publications

References 48 publications

A novel autophagy modulator 6-Bio ameliorates SNCA/α-synuclein toxicity

A novel autophagy modulator 6-Bio ameliorates SNCA/α-synuclein toxicity

Impairment of Wnt/β-catenin signaling in blood cells of patients with severe cavitary pulmonary tuberculosis

Wnt3A Induces GSK‐3β Phosphorylation and β‐Catenin Accumulation Through RhoA/ROCK

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