scholarly journals Frequent accumulation of nuclear E-cadherin and alterations in the Wnt signaling pathway in esophageal squamous cell carcinomas

2007 ◽  
Vol 21 (3) ◽  
pp. 271-281 ◽  
Author(s):  
Sima Salahshor ◽  
Richard Naidoo ◽  
Stefano Serra ◽  
Warren Shih ◽  
Ming-Sound Tsao ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Wnt Signaling Pathway ◽  
Squamous Cell Carcinomas ◽  
Esophageal Squamous Cell Carcinomas ◽  
E Cadherin

scholarly journals The Significance of the Dysregulation of Canonical Wnt Signaling in Head and Neck Squamous Cell Carcinomas

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 723 ◽  
Author(s):  
Jarosław Paluszczak
Keyword(s):  
Cell Proliferation ◽  
Head And Neck Cancer ◽  
Wnt Signaling ◽  
Head And Neck ◽  
Neck Cancer ◽  
Squamous Cell ◽  
Wnt Signaling Pathway ◽  
Squamous Cell Carcinomas ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

The knowledge about the molecular alterations which are found in head and neck squamous cell carcinomas (HNSCC) has much increased in recent years. However, we are still awaiting the translation of this knowledge to new diagnostic and therapeutic options. Among the many molecular changes that are detected in head and neck cancer, the abnormalities in several signaling pathways, which regulate cell proliferation, cell death and stemness, seem to be especially promising with regard to the development of targeted therapies. Canonical Wnt signaling is a pathway engaged in the formation of head and neck tissues, however it is not active in adult somatic mucosal cells. The aim of this review paper is to bring together significant data related to the current knowledge on the mechanisms and functional significance of the dysregulation of the Wnt/β-catenin pathway in head and neck tumors. Research evidence related to the role of Wnt signaling activation in the stimulation of cell proliferation, migration and inhibition of apoptosis in HNSCC is presented. Moreover, its role in promoting stemness traits in head and neck cancer stem-like cells is described. Evidence corroborating the hypothesis that the Wnt signaling pathway is a very promising target of novel therapeutic interventions in HNSCC is also discussed.

scholarly journals Roles of the Wnt Signaling Pathway in Head and Neck Squamous Cell Carcinoma

2021 ◽  
Vol 7 ◽  
Author(s):  
Jing Xie ◽  
Li Huang ◽  
You-Guang Lu ◽  
Da-Li Zheng
Keyword(s):  
Squamous Cell Carcinoma ◽  
Wnt Signaling ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Wnt Pathway ◽  
Wnt Signaling Pathway ◽  
Neck Squamous Cell Carcinoma ◽  
Upstream Gene

Head and neck squamous cell carcinoma (HNSCC) is the most common type of head and neck tumor. It is a high incidence malignant tumor associated with a low survival rate and limited treatment options. Accumulating conclusions indicate that the Wnt signaling pathway plays a vital role in the pathobiological process of HNSCC. The canonical Wnt/β-catenin signaling pathway affects a variety of cellular progression, enabling tumor cells to maintain and further promote the immature stem-like phenotype, proliferate, prolong survival, and gain invasiveness. Genomic studies of head and neck tumors have shown that although β-catenin is not frequently mutated in HNSCC, its activity is not inhibited by mutations in upstream gene encoding β-catenin, NOTCH1, FAT1, and AJUBA. Genetic defects affect the components of the Wnt pathway in oral squamous cell carcinoma (OSCC) and the epigenetic mechanisms that regulate inhibitors of the Wnt pathway. This paper aims to summarize the groundbreaking discoveries and recent advances involving the Wnt signaling pathway and highlight the relevance of this pathway in head and neck squamous cell cancer, which will help provide new insights into improving the treatment of human HNSCC by interfering with the transcriptional signaling of Wnt.

scholarly journals Effects of microRNA-136 on melanoma cell proliferation, apoptosis, and epithelial–mesenchymal transition by targetting PMEL through the Wnt signaling pathway

2017 ◽  
Vol 37 (5) ◽  
Author(s):  
Jiu-Jiang Wang ◽  
Zhi-Feng Li ◽  
Xiao-Jing Li ◽  
Zhao Han ◽  
Ling Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Melanoma Cell ◽  
Epithelial Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Melanoma Cells ◽  
Model Group ◽  
Mesenchymal Transition ◽  
E Cadherin

The study aims to evaluate the effects of miR-136 on the proliferation, apoptosis, and epithelial–mesenchymal transition (EMT) of melanoma cells by targetting premelanosome protein (PMEL) through the Wnt signaling pathway. After establishment of melanoma mouse models, melanoma (model group) and normal tissues (normal group) were collected. Immunohistochemistry was performed to determine PMEL protein concentration. Mouse melanoma cells were assigned into control, blank, negative control (NC), miR-136 mimics, miR-136 inhibitors, siRNA-PMEL, and miR-136 inhibitors + siRNA-PMEL, LiC1 (Wnt signaling pathway activator), and siRNA-PMEL+ LiCl groups. MTT, Scratch test, Transwell assay, and flow cytometry were performed to measure cell proliferation, migration, invasion, and apoptosis. Quantitative real-time PCR (qRT-PCR) and Western blotting were performed to evaluate miR-136, PMEL, β-catenin, Wnt3a, Bcl-2, Bax, Caspase, E-cadherin, and N-cadherin expressions. PMEL is highly expressed in melanoma tissues. MiR-136, Bax, Caspase, and E-cadherin expressions decreased in the model group, whereas PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin expressions increased. Bax, Caspase, and E-cadherin expressions increased in the miR-136 mimics and siRNA-PMEL groups, whereas the expressions decreased in the miR-136 inhibitors group and LiC1 group. PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin expressions, cell proliferation, migration, and invasion decreased, and the apoptosis rate inceased in the miR-136 mimics and siRNA-PMEL groups; whereas the tendencies were opposite to those in the miR-136 inhibitors group and LiC1 group. In the siRNA-PMEL+ LiCl group, PMEL expression decreased. These findings indicated that overexpression of miR-136 inhibits melanoma cell EMT, proliferation, migration, invasion, and promotes apoptosis by targetting PMEL through down-regulation of the Wnt signaling pathway.

scholarly journals Transgelin Inhibits the Malignant Progression of Esophageal Squamous Cell Carcinomas by Regulating Epithelial–Mesenchymal Transition

2021 ◽  
Vol 11 ◽  
Author(s):  
Boli Yang ◽  
Qiuyu Chen ◽  
Changshan Wan ◽  
Siyuan Sun ◽  
Lanping Zhu ◽  
...  
Keyword(s):  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Squamous Cell Carcinomas ◽  
Malignant Progression ◽  
Expression Level ◽  
Migration And Invasion ◽  
Control Group ◽  
Mesenchymal Transition ◽  
Esophageal Squamous Cell Carcinomas ◽  
E Cadherin

ObjectiveThis article investigates the role of Transgelin (TAGLN) in the epithelial–mesenchymal transition (EMT) of esophageal squamous cell carcinomas (ESCC) and its possible mechanism of inhibiting the invasion of these cancers.MethodsTissue specimens and clinical information of patients with ESCC were collected to analyze the relationship between Transgelin expression level and prognosis of patients with ESCC. Transgelin siRNA was used to knock down Transgelin expression. The expression of Transgelin in Eca-109 and KYSE-150 cells was overexpressed by Transgelin-overexpressing plasmid. The effects of Transgelin overexpression and knockdown on the proliferation of Eca-109 and KYSE-150 cells were examined by Transwell chamber, scratch assay, and CCK-8 cell activity assay. RT-PCR and Western blot were used to detect the effect of Transgelin overexpression or knockdown on the mRNA and protein expressions of E-cadherin and Vimentin. TCGA data were used to analyze Transgelin co-expressed genes and further study the GO and KEGG enrichment analysis results under the influence of Transgelin.ResultsThe expression of Transgelin was low in ESCC, and its expression level was positively correlated with the prognosis of patients with ESCC. The targeted Transgelin siRNA and Transgelin-overexpressing plasmid can effectively regulate the expression of Transgelin mRNA and protein in Eca-109 and KYSE-150 cells. After overexpression of Transgelin, the invasion and proliferation abilities of Eca-109 and KYSE-150 cells were significantly decreased compared with those of the control group (P < 0.05). However, Transgelin knockdown could promote the proliferation, migration, and invasion of ESCC cells. The overexpression of Transgelin inhibits EMT in ESCC. With the increase of Transgelin expression in Eca-109 and KYSE-150 cells, the expression of E-cadherin increased, while the expression of Vimentin decreased, and the difference was statistically significant (P < 0.05).ConclusionTransgelin can inhibit the malignant progression of ESCC by inhibiting the occurrence of EMT.

scholarly journals E-Cadherin/β-Catenin Complex and the Epithelial Barrier

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Xinrui Tian ◽  
Zhuola Liu ◽  
Bo Niu ◽  
Jianlin Zhang ◽  
Thian Kui Tan ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Epithelial Barrier ◽  
Aberrant Expression ◽  
Mesenchymal Transition ◽  
A Cell ◽  
Suppressive Action ◽  
E Cadherin

E-Cadherin/β-catenin complex plays an important role in maintaining epithelial integrity and disrupting this complex affect not only the adhesive repertoire of a cell, but also the Wnt-signaling pathway. Aberrant expression of the complex is associated with a wide variety of human malignancies and disorders of fibrosis resulting from epithelial-mesenchymal transition. These associations provide insights into the complexity that is likely responsible for the fibrosis/tumor suppressive action of E-cadherin/β-catenin.

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