scholarly journals Air pollution-regulated E-cadherin mediates contact inhibition of proliferation via the hippo signaling pathways in emphysema

2021 ◽  
pp. 109763
Author(s):  
Jer-Hwa Chang ◽  
Yueh-Lun Lee ◽  
Vincent Laiman ◽  
Chia-Li Han ◽  
Yu-Teng Jheng ◽  
...  
Keyword(s):  
Air Pollution ◽  
Signaling Pathways ◽  
Contact Inhibition ◽  
Hippo Signaling ◽  
Inhibition Of Proliferation ◽  
E Cadherin

scholarly journals Air Pollution-Regulated E-Cadherin Mediates Contact Inhibition of Proliferation via the Hippo Signaling Pathways in Emphysema

2021 ◽  
Author(s):  
Jer-Hwa Chang ◽  
Yueh-Lun Lee ◽  
Vincent Laiman ◽  
Chia-Li Han ◽  
Yu-Teng Jheng ◽  
...  
Keyword(s):  
Air Pollution ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Interaction Network ◽  
Contact Inhibition ◽  
Hippo Signaling ◽  
Inhibition Of Proliferation ◽  
Hippo Signaling Pathway ◽  
Alveolar Epithelial ◽  
E Cadherin

Abstract Background: Air pollution has been linked to emphysema in chronic obstruction pulmonary disease (COPD). However, the underlying mechanisms in the development of emphysema due to air pollution remain unclear. The objective of this study was to investigate the role of components of the Hippo signaling pathway for E-cadherin-mediated contact inhibition of proliferation in the lungs after air pollution exposure. E-Cadherin-mediated contact inhibition of proliferation via the Hippo signaling pathway was investigated in Sprague-Dawley (SD) rats whole-body exposed to air pollution, and in alveolar epithelial A549 cells exposed to diesel exhaust particles (DEPs), E-cadherin-knockdown, and high-mobility group box 1 (HMGB1) treatment. Underlying epithelial differentiation, apoptosis, and senescence were also examined, and the interaction network among these proteins was examined. COPD lung sections were used to confirm the observations in rats. Results: Expressions of HMGB1 and E-cadherin were negatively regulated in the lungs and A549 cells by air pollution, and this was confirmed by knockdown of E-cadherin and by treating A549 cells with HMGB1. Depletion of phosphorylated (p)-Yap occurred after exposure to air pollution and E-cadherin-knockdown, which resulted in decreases of SPC and T1α. Exposure to air pollution and E-cadherin-knockdown respectively downregulated p-Sirt1 and increased p53 levels in the lungs and in A549 cells. Moreover, the protein interaction network suggested that E-cadherin is a key activator in regulating Sirt1 and p53, as well as alveolar epithelial cell differentiation by SPC and T1α. Consistently, downregulation of E-cadherin, p-Yap, SPC, and T1α was observed in COPD alveolar regions with particulate matter (PM) deposition. Conclusions: Our results indicated that E-cadherin-mediated cell-cell contact directly regulates the Hippo signaling pathway to control differentiation, cell proliferation, and senescence due to air pollution. Exposure to air pollution may initiate emphysema in COPD patients.

scholarly journals The Molecular Mechanism of Epithelial–Mesenchymal Transition for Breast Carcinogenesis

Biomolecules ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 476 ◽  
Author(s):  
Chia-Jung Li ◽  
Pei-Yi Chu ◽  
Giou-Teng Yiang ◽  
Meng-Yu Wu
Keyword(s):  
Epithelial Cells ◽  
Tumor Progression ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Inhibition Of Proliferation ◽  
Mesenchymal Transition

The transforming growth factor-β (TGF-β) signaling pathway plays multiple regulatory roles in the tumorigenesis and development of cancer. TGF-β can inhibit the growth and proliferation of epithelial cells and induce apoptosis, thereby playing a role in inhibiting breast cancer. Therefore, the loss of response in epithelial cells that leads to the inhibition of cell proliferation due to TGF-β is a landmark event in tumorigenesis. As tumors progress, TGF-β can promote tumor cell invasion, metastasis, and drug resistance. At present, the above-mentioned role of TGF-β is related to the interaction of multiple signaling pathways in the cell, which can attenuate or abolish the inhibition of proliferation and apoptosis-promoting effects of TGF-β and enhance its promotion of tumor progression. This article focuses on the molecular mechanisms through which TGF-β interacts with multiple intracellular signaling pathways in tumor progression and the effects of these interactions on tumorigenesis.

scholarly journals Honeybee (Apis mellifera) Maternal Effect Causes Alternation of DNA Methylation Regulating Queen Development

Sociobiology ◽  
2021 ◽  
Vol 68 (1) ◽  
pp. 5935
Author(s):  
Xu Jiang He ◽  
Hao Wei ◽  
Wu Jun Jiang ◽  
Yi Bo Liu ◽  
Xiao Bo Wu ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Apis Mellifera ◽  
Signaling Pathways ◽  
Maternal Effect ◽  
Caste Differentiation ◽  
Hippo Signaling ◽  
Thorax Length ◽  
Queen Cell ◽  
Epigenetic Analysis ◽  
Worker Caste

Queen-worker caste dimorphism is a typical trait for honeybees (Apis mellifera). We previously showed a maternal effect on caste differentiation and queen development, where queens emerged from queen-cell eggs (QE) had higher quality than queens developed from worker cell eggs (WE). In this study, newly-emerged queens were reared from QE, WE, and 2-day worker larvae (2L). The thorax size and DNA methylation levels of queens were measured. We found that queens emerging from QE had significantly larger thorax length and width than WE and 2L. Epigenetic analysis showed that QE/2L comparison had the most different methylated genes (DMGs, 612) followed by WE/2L (473), and QE/WE (371). Interestingly, a great number of DMGs (42) were in genes belonging to mTOR, MAPK, Wnt, Notch, Hedgehog, FoxO, and Hippo signaling pathways that are involved in regulating caste differentiation, reproduction and longevity. This study proved that honeybee maternal effect causes epigenetic alteration regulating caste differentiation and queen development.

scholarly journals E-cadherin in contact inhibition and cancer

Oncogene ◽  
2018 ◽  
Vol 37 (35) ◽  
pp. 4769-4780 ◽  
Author(s):  
Alisha M. Mendonsa ◽  
Tae-Young Na ◽  
Barry M. Gumbiner
Keyword(s):  
Contact Inhibition ◽  
E Cadherin

scholarly journals TEADs, Yap, Taz, Vgll4s transcription factors control the establishment of Left-Right asymmetry in zebrafish

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Jonathan Fillatre ◽  
Jean-Daniel Fauny ◽  
Jasmine Alexandra Fels ◽  
Cheng Li ◽  
Mary Goll ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Signaling Pathways ◽  
Transcriptional Control ◽  
Hippo Pathway ◽  
Hippo Signaling ◽  
Zebrafish Model ◽  
Transcription Cofactor ◽  
Expression Of Genes ◽  
Epigenetic Programming ◽  
Left Right Asymmetry

In many vertebrates, establishment of Left-Right (LR) asymmetry results from the activity of a ciliated organ functioning as the LR Organizer (LRO). While regulation of the formation of this structure by major signaling pathways has been described, the transcriptional control of LRO formation is poorly understood. Using the zebrafish model, we show that the transcription factors and cofactors mediating or regulating the transcriptional outcome of the Hippo signaling pathway play a pivotal role in controlling the expression of genes essential to the formation of the LRO including ligands and receptors of signaling pathways involved in this process and most genes required for motile ciliogenesis. Moreover, the transcription cofactor, Vgll4l regulates epigenetic programming in LRO progenitors by controlling the expression of writers and readers of DNA methylation marks. Altogether, our study uncovers a novel and essential role for the transcriptional effectors and regulators of the Hippo pathway in establishing LR asymmetry.

scholarly journals MicroRNA-338-3p suppresses ovarian cancer cells growth and metastasis: implication of Wnt/catenin beta and MEK/ERK signaling pathways

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Ruitao Zhang ◽  
Huirong Shi ◽  
Fang Ren ◽  
Wei Feng ◽  
Yuan Cao ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Target Genes ◽  
Erk Signaling ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Inhibition Of Proliferation ◽  
Mesenchymal Transition ◽  
Biomedical Databases

Abstract Background Downregulation of microRNA-338-3p (miR-338-3p) was detected in many malignant tumors, which indicated miR-338-3p might serve as a role of antioncogene in those cancers. The present study aimed to explore the roles of miR-338-3p in the growth and metastasis of ovarian cancer cells and elaborate the underlying possible molecular mechanism. Methods Multiply biomedical databases query and KEGG pathway enrichment assay were used to infilter possible target genes and downstream pathways regulated by miR-338-3p. Overexpression miR-338-3p lentiviral vectors were transfected into ovarian cancer OVCAR-3 and OVCAR-8 cells, cell proliferation, migration and invasion were analyzed by MTT, colony formation, transwell, Matrigel assay and xenograft mouse model. One 3′-untranslated regions (UTRs) binding target gene of miR-338-3p, MACC1 (MET transcriptional regulator MACC1), and its regulated gene MET and downstream signaling pathway activities were examined by western blot. Results Biomedical databases query indicated that miR-338-3p could target MACC1 gene and regulate Met, downstream Wnt/Catenin beta and MEK/ERK pathways. Rescue of miR-338-3p could inhibit the proliferation, migration and invasion of ovarian cancer cells, and suppress the growth and metastasis of xenograft tumor. Restoration of miR-338-3p could attenuate MACC1 and Met overexpression induced growth, epithelial to mesenchymal transition (EMT) and activities of Wnt/Catenin beta and MEK/ERK signaling in vitro and in vivo. Conclusions The present data indicated that restoration of miR-338-3p could suppress the growth and metastasis of ovarian cancer cells, which might due to the inhibition of proliferation and EMT induced by MACC1, Met and its downstream Wnt/Catenin beta and MEK/ERK signaling pathways.

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