Modulation of E-cadherin expression promotes migration ability of esophageal cancer cells

Li, Shujun; Qin, Xuebo; Chai, Song; Qu, Chun-Ying; Wang, Xiaolu; Zhang, Helin

doi:10.1038/srep21713

Cited by 25 publications

(22 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One of the hallmarks of EMT is the functional loss of E‐cadherin, which is associated with epithelial‐to‐mesenchymal transition in cancer . A previous study demonstrated that reduced E‐cadherin decreases the strength of cellular adhesion, resulting in increased cellular motility; however, the overexpression of E‐cadherin was sufficient to prevent migration. Therefore, E‐cadherin plays a critical role in migratory ability.…”

Section: Discussionmentioning

confidence: 98%

“…To investigate the mechanism by which oridonin increased the expression of E‐cadherin in this study, the transcription factors snail and slug were investigated as these two proteins bind to the E‐cadherin promoter to suppress E‐cadherin expression . The results showed that the expression of snail and slug was significantly decreased by oridonin when compared with their expression in the control group . Furthermore, the expression of vimentin was significantly decreased after the application of oridonin.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Oridonin inhibits the migration and epithelial‐to‐mesenchymal transition of small cell lung cancer cells by suppressing FAK‐ERK1/2 signalling pathway

Bi²,

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

Small cell lung cancer (SCLC) is a severe malignant with high morbidity; however, few effective and secure therapeutic strategy is used in current clinical practice. Oridonin is a small molecule from the traditional Chinese herb Rabdosia rubescens. This study mainly aimed to investigate the role of oridonin on inhibiting the process of H1688, a kind of small cell lung cancer cells from human. Oridonin could suppress H1688 cell proliferation and induce their apoptosis in a high dosage treatment (20 μmol/L).Meanwhile, cell migration was suppressed by oridonin (5 and 10 μmol/L) that did not affect cell proliferation and apoptosis. The expression level of E-cadherin was significantly increased, and the expression of vimentin, snail and slug was reduced after administration of oridonin. These expression changes were associated with the suppressed integrin β1, phosphorylation of focal adhesion kinase (FAK) and ERK1/2.In addition, oridonin (5 and 10 mg/kg) inhibited tumour growth in a nude mouse model; however, HE staining revealed a certain degree of cytotoxicity in hepatic tissue after treatment oridonin (10 mg/kg). Furthermore, the concentration of alanine aminotransferase (ALP) was significantly increased and lactate dehydrogenase (LDH) was reduced after oridonin treatment (10 mg/kg). Immunohistochemical analysis further revealed that oridonin increased E-cadherin expression and reduced vimentin and phospho-FAK levels in vivo. These findings indicated that oridonin can inhibit the migration and epithelial-to-mesenchymal transition (EMT) of SCLC cells by suppressing the FAK-ERK1/2 signalling pathway. Thus, oridonin may be a new drug candidate to offer an effect of anti-SCLC with relative safety. K E Y W O R D Sfocal adhesion kinase, migration, oridonin, small cell lung cancer | 4481 XU et al.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Oridonin inhibits the migration and epithelial‐to‐mesenchymal transition of small cell lung cancer cells by suppressing FAK‐ERK1/2 signalling pathway

Bi²,

et al. 2020

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…Insert A is generally linked to localization of NLGN1 at inhibitory synapses, whereas insert B localizes NLGN1 at excitatory synapses (Chih, Gollan, & Scheiffele, ). Additionally to an increase in its mRNA level in Clock knock‐down cell culture, E‐cadherin expression is decreased by Per2 overexpression in esophageal cancer cells (Li et al., , ). This overexpression of Per2 increases the level of histone deacetylase HDAC1 at E‐cadherin promoter, which then increases the recruitment of repressors (Li et al., ).…”

Section: Adhesion and Scaffolding Moleculesmentioning

confidence: 99%

Transcriptional control of synaptic components by the clock machinery

Hannou

Roy

Roig

et al. 2019

Eur J of Neuroscience

View full text Add to dashboard Cite

Circadian rhythms are generated in mammals by a central clock located in the suprachiasmatic nucleus of the hypothalamus, which regulates the homeostasis of many biological processes. At the molecular level, the regulation of circadian rhythms is under the control of transcriptional‐translational feedback loops composed of clock factors, including transcription factors. In the brain, synaptic plasticity has been shown to vary with a 24‐h rhythm. Also, when measured at a given time‐of‐day, synaptic plasticity has been observed to be disrupted by dysregulation of clock factors. This could suggest a regulation of synaptic functions by the clock machinery. Interestingly, many studies provide support for direct and indirect transcriptional regulation by core clock factors, including rhythmic gene expression, for a variety of synaptic components. Indeed, the gene of several neuropeptides, neurotransmitter regulators, receptors and transporters, ion channels, vesicle proteins, and adhesion and scaffolding molecules present evidence to be clock‐controlled. We here present, while considering different regions of the mammalian brain, an overview of the extent of the transcriptional control of synaptic components by the clock machinery.

show abstract

“…It is mentioned as a typical tumor suppressor gene and plays a critical role in carcinogenesis. Loss expression of CDH1 enables disaggregation of cancer cells from one another and increases their metastatic potential [11,12]. However, the pattern of CDH1 expression and its clinical implication remain to be elucidated in AML.…”

Section: Introductionmentioning

confidence: 97%

CDH1 (E-cadherin) expression independently affects clinical outcome in acute myeloid leukemia with normal cytogenetics

Zhang

Zhou

et al. 2016

Clinical Chemistry and Laboratory Medicine (CCLM)

View full text Add to dashboard Cite

show abstract

Modulation of E-cadherin expression promotes migration ability of esophageal cancer cells

Cited by 25 publications

References 28 publications

Oridonin inhibits the migration and epithelial‐to‐mesenchymal transition of small cell lung cancer cells by suppressing FAK‐ERK1/2 signalling pathway

Oridonin inhibits the migration and epithelial‐to‐mesenchymal transition of small cell lung cancer cells by suppressing FAK‐ERK1/2 signalling pathway

Transcriptional control of synaptic components by the clock machinery

CDH1 (E-cadherin) expression independently affects clinical outcome in acute myeloid leukemia with normal cytogenetics

Contact Info

Product

Resources

About