Autophagy eliminates cytoplasmic β-catenin and NICD to promote the cardiac differentiation of P19CL6 cells

Jia, Zhonghua; Wang, Jiaji; Wang, Weiping; Tian, Yuyao; XiangWei, Wenshu; Chen, Ping; Ma, Kangtao; Zhou, Chen

doi:10.1016/j.cellsig.2014.07.028

Cited by 59 publications

(48 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies have shown that β-catenin signaling may play a role in autophagy in some models [10,11,12,13,14,15], whereas its involvement in autophagy in prostate cancer cells has not been addressed.…”

Section: Discussionmentioning

confidence: 99%

“…However, our knowledge on these contexts is rather limited. Recent studies have shown that Wnt/β-catenin signaling plays a role in autophagy in some models [10,11,12,13,14,15], but the involvement of this pathway in prostate cancer has not been reported. The Wnt signaling pathways are a group of signaling pathways that have been catalogued as the canonical Wnt pathway, the noncanonical planar cell polarity pathway and the noncanonical Wnt/calcium pathway.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling

Lin

Feng

Shao-liang

et al. 2015

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Autophagy is a cellular degradation process for the recycling of damaged or superfluous intracellular compartments to provide an alternative energy source during periods of metabolic stress for maintaining cell homeostasis and viability. Although autophagy in different contexts have been shown to use similar signaling pathways, the exact molecular regulation of autophagy has been found to be cell-type dependent. Methods: We used rapamycin to trigger autophagy and used nitric oxide (NO) to inhibit autophagy in prostate cancer cells. IWP-2 was used to inhibit β-catenin signaling. Autophagy-associated proteins were examined by Western blot. Results: We found that nitric oxide (NO), a potent cellular messenger, impaired rapamycin-induced autophagy in prostate cancer cells. Further analyses showed that NO induced nuclear accumulation of β-catenin, a key factor of Wnt signaling pathway, to inhibit autophagy in prostate cancer cells. Conclusions: We demonstrate involvement of β-catenin signaling in the regulation of autophagy of prostate cancer cells. Our results shed light on a previously unappreciated β-catenin signaling pathway for regulating autophagy in prostate cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling

Lin

Feng

Shao-liang

et al. 2015

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…These results are consistent with previous reports showing the loss of autophagy leads to the activation of the Notch signaling in Drosophila oogenesis 25 and autophagy eliminates cytoplasmic NICD to promote cardiac differentiation. 26 Autophagy is activated by mammalian target of rapamycin protein kinase pathway (mTOR). 41 mTOR is a center of autophagy regulation molecule, which is inhibited autophagy associated gene(ATG) to regulate autophagy.…”

Section: Discussionmentioning

confidence: 99%

“…25,26 Therefore, we investigate whether Notch1 signaling pathway can be regulated by autophagy during the biliary differentiation of WB-F344 cells. We also examine the effect of 2 autophagy stimuli, the mTOR inhibitor rapamycin and nutrient deprivation medium, on the biliary differentiation of WB-F344 cells.…”

Section: Autophagy Inhibits Notch1 Signaling Pathway During the Biliamentioning

confidence: 99%

“…25 In cardiac differentiation, Autophagy eliminates cytoplasmic NICD to promote cardiac differentiation. 26 However, whether autophagy regulates Notch signaling pathways in biliary differentiation is not well understood. Here we report that autophagy regulates biliary differentiation of hepatic progenitor cells through Notch1 signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Autophagy regulates biliary differentiation of hepatic progenitor cells through Notch1 signaling pathway

et al. 2016

View full text Add to dashboard Cite

Autophagy plays important roles in self-renewal and differentiation of stem cells. Hepatic progenitor cells (HPCs) are thought to have the ability of self-renewal as well as possess a bipotential capacity, which allows them to differentiate into both hepatocytes and bile ductular cells. However, how autophagy contributes to self-renewal and differentiation of hepatic progenitor cells is not well understood. In this study, we use a well-established rat hepatic progenitor cell lines called WB-F344, which is treated with 3.75 mM sodium butyrate (SB) to promote the differentiation of WB-F344 along the biliary phenotype. We found that autophagy was decreased in the early stage of biliary differentiation, and maintained a low level at the late stage. Activation of autophagy by rapamycin or starvation suppressed the biliary differentiation of WB-F344. Further study reported that autophagy inhibited Notch1 signaling pathway, which contributed to biliary differentiation and morphogenesis. In conclusions, autophagy regulates biliary differentiation of hepatic progenitor cells through Notch1 signaling pathway.

show abstract

ErbB2‐NOTCH1 axis controls autophagy in cardiac cells

Fortini,

Vieceli Dalla Sega,

Lazzarini

et al. 2024

BioFactors

View full text Add to dashboard Cite

Although the epidermal growth factor receptor 2 (ErbB2) and Notch1 signaling pathways have both significant roles in regulating cardiac biology, their interplay in the heart remains poorly investigated. Here, we present evidence of a crosstalk between ErbB2 and Notch1 in cardiac cells, with effects on autophagy and proliferation. Overexpression of ErbB2 in H9c2 cardiomyoblasts induced Notch1 activation in a post‐transcriptional, p38‐dependent manner, while ErbB2 inhibition with the specific inhibitor, lapatinib, reduced Notch1 activation. Moreover, incubation of H9c2 cells with lapatinib resulted in stalled autophagic flux and decreased proliferation, consistent with the established cardiotoxicity of this and other ErbB2‐targeting drugs. Confirming the findings in H9c2 cells, exposure of primary neonatal mouse cardiomyocytes to exogenous neuregulin‐1, which engages ErbB2, stimulated proliferation, and this effect was abrogated by concomitant inhibition of the enzyme responsible for Notch1 activation. Furthermore, the hearts of transgenic mice specifically overexpressing ErbB2 in cardiomyocytes had increased levels of active Notch1 and of Notch‐related genes. These data expand the knowledge of ErbB2 and Notch1 functions in the heart and may allow better understanding the mechanisms of the cardiotoxicity of ErbB2‐targeting cancer treatments.

show abstract

Autophagy eliminates cytoplasmic β-catenin and NICD to promote the cardiac differentiation of P19CL6 cells

Cited by 59 publications

References 37 publications

Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling

Regulation of Autophagy of Prostate Cancer Cells by β-Catenin Signaling

Autophagy regulates biliary differentiation of hepatic progenitor cells through Notch1 signaling pathway

ErbB2‐NOTCH1 axis controls autophagy in cardiac cells

Contact Info

Product

Resources

About