scholarly journals Combination of quercetin and 2-methoxyestradiol inhibits epithelial–mesenchymal transition in PC-3 cell line via Wnt signaling pathway

2021 ◽  
pp. FSO747
Author(s):  
Neeti Sharma ◽  
Piyush W Raut ◽  
Meghna M Baruah ◽  
Akshay Sharma
Keyword(s):  
Wnt Signaling ◽  
Epithelial Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Signaling Proteins ◽  
Rt Pcr ◽  
Mesenchymal Transition ◽  
Promising Therapeutic Approach ◽  
Signaling Components ◽  
Emt Markers

Aim: We have previously reported that quercetin (Qu) regulates epithelial–mesenchymal transition (EMT) by modulating Wnt signaling components. In this study, we investigated the synergistic effect of Qu and 2-methoxyestradiol (2-ME) and the role of Wnt signaling components in regulating EMT in PC-3 cells. Materials & methods: EMT was induced by treating PC-3 cells with TGF-β, followed by evaluation of expression of EMT markers and Wnt signaling proteins in naive, induced and after exposing induced cells to Qu and 2-ME at both gene and protein level by real-time PCR (RT-PCR) and western blot, respectively. Results: Qu and 2-ME synergistically downregulated mesenchymal markers with simultaneous upregulation of epithelial markers. Wnt signaling proteins expression was also downregulated by Qu and 2-ME in TGF-β-induced EMT in PC-3 cells. Conclusion: Thus, combination therapy of Qu and 2-ME could be a new promising therapeutic approach for the treatment of prostate cancer.

scholarly journals Wnt Signaling Pathway Is among the Drivers of Liver Metastasis

Livers ◽  
2021 ◽  
Vol 1 (4) ◽  
pp. 180-200
Author(s):  
Ivana Samaržija
Keyword(s):  
Liver Metastasis ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Metastasis Formation ◽  
Mesenchymal Transition ◽  
Cancer Types ◽  
The Many

Liver metastasis, originating either from a primary liver or other cancer types, represent a large cancer-related burden. Therefore, studies that add to better understanding of its molecular basis are needed. Herein, the role of the Wnt signaling pathway in liver metastasis is outlined. Its role in hepatocellular carcinoma (HCC) epithelial-mesenchymal transition (EMT), motility, migration, metastasis formation, and other steps of the metastatic cascade are presented. Additionally, the roles of the Wnt signaling pathway in the liver metastasis formation of colorectal, breast, gastric, lung, melanoma, pancreatic, and prostate cancer are explored. The special emphasis is given to the role of the Wnt signaling pathway in the communication between the many of the components of the primary and secondary cancer microenvironment that contribute to the metastatic outgrowth in the liver. The data presented herein are a review of the most recent publications and advances in the field that add to the idea that the Wnt pathway is among the drivers of liver metastasis and that its targeting could potentially relieve liver metastasis–related complications.

WNT2b Activates Epithelial-mesenchymal Transition Through FZD4: Relevance in Penetrating Crohn´s Disease

2019 ◽  
Vol 14 (2) ◽  
pp. 230-239 ◽  
Author(s):  
Dolores Ortiz-Masià ◽  
Pedro Salvador ◽  
Dulce C Macias-Ceja ◽  
Laura Gisbert-Ferrándiz ◽  
Juan V Esplugues ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Fistula Formation ◽  
Rt Pcr ◽  
Intestinal Tissue ◽  
Mesenchymal Transition ◽  
Ht29 Cells ◽  
Wnt Ligands ◽  
Emt Markers

Abstract Background and Aims Epithelial-mesenchymal transition [EMT] has been related to fibrosis and fistula formation, common complications associated with Crohn´s disease [CD]. The WNT signalling pathway mediates EMT, and specific WNT/FZD interactions have been related to the activation of this process in several diseases. We aim to analyse the relevance of EMT and WNT ligands and receptors in the penetrating behaviour of CD. Methods Intestinal surgical resections were obtained from control and CD patients with a stenotic or penetrating behaviour. Fibrosis was determined by the histological analysis of collagen deposition and EMT by confocal microscopy. The expression of WNT ligands, inhibitors, and FZD receptors was analysed by RT-PCR, WB, IH, and IF studies. The effects of WNT2b and the role of FZD4 in EMT were analysed in HT29 epithelial cells. Results Fibrosis and expression of EMT markers were detected in samples from CD patients irrespective of the clinical behaviour. However, an increased colocalisation of E-CADHERIN and VIMENTIN, an increased number of cells expressing WNT2b, and a higher expression of FZD4 and WNT2b/FZD4 interaction, were detected in intestinal tissue from the penetrating compared with the stenotic CD behaviour. WNT2b induced EMT in HT29 cells through FZD4 activation. Conclusions An increased EMT, associated with increased WNT2b/FZD4 interaction, was detected in intestinal tissue from CD patients with a penetrating behaviour. WNT2b, through FZD4 activation, induces EMT in vitro which points to a novel pharmacological target to prevent intestinal penetrating complications of CD.

scholarly journals miR-22 Suppresses Epithelial-Mesenchymal Transition by Modulating Snail and MAPK1 in Hepatocellular Carcinoma

2020 ◽  
Author(s):  
Cheng-Gong Liao ◽  
Zhi Qu ◽  
Zao-Xia Guo ◽  
Xiao-Hua Liang ◽  
Ling-Min Kong
Keyword(s):  
Real Time ◽  
Epithelial Mesenchymal Transition ◽  
Mitogen Activated Protein Kinase ◽  
Luciferase Reporter ◽  
Rt Pcr ◽  
Mesenchymal Transition ◽  
Normal Tissues ◽  
Mitogen Activated Protein ◽  
Emt Markers

Abstract Background: Recently studies have reported that miR-22 plays an important role in epithelial-mesenchymal transition (EMT) of many human cancers. However, the involvement of miR-22 in hepatocellular carcinomas (HCC) EMT progression has not been investigated. Methods: We measured miR-22 expression level in 38 paired of HCC and matched normal tissues by real-time quantitative RT-PCR. Then, we performed morphological analysis and immunofluorescence to observe the role of miR-22 in HCC EMT progression. The expression of EMT markers were detected by real-time RT-PCR and western blot. The regulation role of miR-22 on Snail, mitogen-activated protein kinase 1(MAPK1) and slug were determined by luciferase reporter assay. The expression of Snail and MAPK1 were also detected by real-time quantitative RT-PCR in HCC and normal tissues. Results: We found that the expression of miR-22 in HCC tissues were much lower than that in normal control. The expression of miR-22 was inversely correlated with HCC metastatic ability. Then, we found that overexpression of miR-22 could inhibit HCC EMT. Importantly, miR-22 is found to inhibit cell motility by directly targeting both Snail and MAPK1. Furthermore, the suppression role of miR-22 in HCC EMT could be blocked by Snail and MAPK1 overexpression. Additionally, the expression of Snail and MAPK1 were inversely correlated with miR-22 expression in HCC tissues. Conclusion: Our results suggested that miR-22 was downexpressed in HCC tissues and inhibited HCC EMT through downregulating Snail and MAPK1 which may provide a new bio-target for HCC therapy.

Diallyl disulphide suppresses the cannonical Wnt signaling pathway and reverses the fibronectin-induced epithelial mesenchymal transition of A549 lung cancer cells

2019 ◽  
Vol 10 (1) ◽  
pp. 191-202 ◽  
Author(s):  
Bornita Das ◽  
Dona Sinha
Keyword(s):  
Lung Cancer ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Lung Cancer Cells ◽  
Mesenchymal Transition ◽  
A549 Lung

DADS reflected the potential of reversal of FN-induced EMT by inhibition of Wnt signaling in A549 lung cancer cells.

215 SNAIL AND SLUG, MARKERS OF EPITHELIAL MESENCHYMAL TRANSITION, APPEARED TO BE ALTERED BY ALKYL-PHENOLS, BISPHENOL A AND NONYL-PHENOL, IN OVARIAN CANCER CELLS EXPRESSING ESTROGEN RECEPTORS

2015 ◽  
Vol 27 (1) ◽  
pp. 198 ◽  
Author(s):  
Y.-S. Kim ◽  
K.-C. Choi
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Ovarian Cancer Cells ◽  
Rt Pcr ◽  
Nonyl Phenol ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Emt Markers ◽  
E Cadherin

The ovary is the important organ to produce oocytes. Any disorder will affect embryo production. Ovarian cancer is one of gynecologic cancers in women which can affect ovarian functions. Oestradiol (E2) may be involved in ovarian cell growth and epithelial-mesenchymal transition (EMT) for diverse functions. EMT is an important process in embryo development and tumour migration or progression. Bis-phenol A (BPA) and nonyl-phenol (NP) have an estrogenic property, which can be suspected as endocrine disrupting chemicals (EDC). In this study, it has been examined whether BPA and NP can cause EMT process and migration in BG-1 ovarian cancer cells. To confirm the effect of these EDCs, BG-1 ovarian cancer cells were cultured and treated with DMSO (0.1%), E2 (10–7 M), BPA (10–6 M) and NP (10–6 M) for 0, 6, and 24 h. The mRNAs were extracted to perform reverse-transcription (RT)-PCR and the changes in the mRNA expressions were analysed by ANOVA test. Following treatments with BPA and NP, alterations of EMT markers; that is, vimentin and E-cadherin, were examined at mRNA levels by RT-PCR. The levels of vimentin were up-regulated by E2, BPA, or NP in a time-dependent manner. In addition, transcriptional factors of EMT response, i.e. snail and slug, were enhanced by these treatments more than 2 times. BG-1 cells were exposed to these EDCs for 0, 24, and 48 h. Vimentin and snail proteins were induced by E2, BPA, or NP, while the expression of E-cadherin was decreased by them. To reveal that this EMT response is affected by oestrogen receptor (ER), the cells were treated with these EDCs in the presence of an ER antagonist, ICI 182 780 (10–6 M). Treatment with ICI 182 780 reversed EDC-induced alteration of these EMT markers, E-cadherin, vimentin, and snail. Since EMT response can cause metastasis, a scratch assay was performed to show migration caused by BPA or NP. BPA or E2 enhanced migratory capability of these BG-1 cells. Taken together, these results indicate that BPA and NP, potential EDC, may have an ability to influence ovarian cancer metastasis via regulating snail and slug genes in ER-positive ovarian cancers. In a future study, their effects in inducing EMT and migration will be tested in a xenograft mouse model.This work was supported by a grant from the Next-Generation BioGreen 21 Program (no. PJ009599), Rural Development Administration, Republic of Korea.

scholarly journals The Role of Carcinogenesis-Related Biomarkers in the Wnt Pathway and Their Effects on Epithelial–Mesenchymal Transition (EMT) in Oral Squamous Cell Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 555 ◽  
Author(s):  
Yunpeng Bai ◽  
Jingjing Sha ◽  
Takahiro Kanno
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Wnt Signaling ◽  
Tumor Progression ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Wnt Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Wnt Signaling Pathway ◽  
Mesenchymal Transition

As oral squamous cell carcinoma (OSCC) can develop from potentially malignant disorders (PMDs), it is critical to develop methods for early detection to improve the prognosis of patients. Epithelial–mesenchymal transition (EMT) plays an important role during tumor progression and metastasis. The Wnt signaling pathway is an intercellular pathway in animals that also plays a fundamental role in cell proliferation and regeneration, and in the function of many cell or tissue types. Specific components of master regulators such as epithelial cadherin (E-cadherin), Vimentin, adenomatous polyposis coli (APC), Snail, and neural cadherin (N-cadherin), which are known to control the EMT process, have also been implicated in the Wnt cascade. Here, we review recent findings on the Wnt signaling pathway and the expression mechanism. These regulators are known to play roles in EMT and tumor progression, especially in OSCC. Characterizing the mechanisms through which both EMT and the Wnt pathway play a role in these cellular pathways could increase our understanding of the tumor genesis process and may allow for the development of improved therapeutics for OSCC.

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