scholarly journals Clinical significance of epithelial–mesenchymal transition–related molecules in lung adenocarcinoma

2019 ◽  
Vol 26 (2) ◽  
Author(s):  
Y. Zhang ◽  
L. F. Wang ◽  
J. H. Gao ◽  
L. Li ◽  
P. Jiang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumour ◽  
Smoking History ◽  
Related Protein ◽  
Vimentin Expression ◽  
Clinicopathologic Characteristics ◽  
Mesenchymal Transition ◽  
The Relationship ◽  
E Cadherin

Background Epithelial–mesenchymal transition (emt) refers to the biologic process in which epithelial cells are transformed into interstitial phenotypes by specific pathways. This transition plays an important biologic role in the process by which epithelium-derived malignant tumour cells acquire the ability to migrate and invade. We explored the relationship between emt-associated molecules and patient-related clinical factors to determine whether any clinical characteristics could be used as biomarkers for emt-related protein alterations in lung cancer—especially lung adenocarcinoma.Methods Tumour specimens were collected from 80 patients with lung adenocarcinoma who underwent surgery or lung biopsy, with 4 patients being evaluated a 2nd time after re-biopsy. Expression of emt-related proteins, including E-cadherin and vimentin, was evaluated by immunohistochemistry. We analyzed the relationship between clinicopathologic characteristics and expression level of the emt markers.Results Positive expression of E-cadherin was observed in 63 patients (79%), and vimentin, in 46 patients (57.5%). No significant relationships between E-cadherin or vimentin expression and smoking history, sex, age, driving gene mutations, or cell differentiation were identified. A significant correlation was observed between vimentin expression and pathologic stage. Of the 4 patients who were evaluated a 2nd time after re-biopsy, 3 showed the same emt-related protein expression status as in the first analysis. In the remaining patient, E-cadherin had changed completely.Conclusions Clinicopathologic factors in cancer patients did not help to diagnose emt status in lung adenocarcinoma; however, TNM stage might be associated with vimentin expression.

scholarly journals Inhibitor of DNA-Binding Protein 4 Suppresses Cancer Metastasis through the Regulation of Epithelial Mesenchymal Transition in Lung Adenocarcinoma

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2021 ◽  
Author(s):  
Chi-Chung Wang ◽  
Yuan-Ling Hsu ◽  
Chi-Jen Chang ◽  
Chia-Jen Wang ◽  
Tzu-Hung Hsiao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Binding ◽  
Lung Adenocarcinoma ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Inhibitor Of Dna Binding ◽  
E Cadherin

Metastasis is a predominant cause of cancer death and the major challenge in treating lung adenocarcinoma (LADC). Therefore, exploring new metastasis-related genes and their action mechanisms may provide new insights for developing a new combative approach to treat lung cancer. Previously, our research team discovered that the expression of the inhibitor of DNA binding 4 (Id4) was inversely related to cell invasiveness in LADC cells by cDNA microarray screening. However, the functional role of Id4 and its mechanism of action in lung cancer metastasis remain unclear. In this study, we report that the expression of Id4 could attenuate cell migration and invasion in vitro and cancer metastasis in vivo. Detailed analyses indicated that Id4 could promote E-cadherin expression through the binding of Slug, cause the occurrence of mesenchymal-epithelial transition (MET), and inhibit cancer metastasis. Moreover, the examination of the gene expression database (GSE31210) also revealed that high-level expression of Id4/E-cadherin and low-level expression of Slug were associated with a better clinical outcome in LADC patients. In summary, Id4 may act as a metastatic suppressor, which could not only be used as an independent predictor but also serve as a potential therapeutic for LADC treatment.

LncRNA CEACAMP8 Regulates the Proliferation, Invasion and Migration of Trophoblast Cells

2019 ◽  
Vol 9 (9) ◽  
pp. 1215-1221
Author(s):  
Li Jie ◽  
Zhangcai Zheng ◽  
Liping Liu ◽  
Yali Liu ◽  
Zhaoyan Meng ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Flow Cytometry Analysis ◽  
Trophoblast Cells ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Qpcr Analysis ◽  
And Migration ◽  
E Cadherin

Preeclampsia (PE) is an idiopathic hypertension syndrome occurring after 20 weeks of gestation. Reports showed that lncRNAs expression was abnormal in preeclampsia. We aimed to investigate the role of lncRNA CEACAMP8 in the proliferation, invasion and migration of trophoblast cells to improve the preeclampsia. The cell transfection effects were determined by RT-qPCR analysis. The proliferation, invasion and migration of HTR-8/SVneo cells were detected by CCK-8 assay, transwell assay and wound healing assay. The flow cytometry analysis analyzed the cell cycle. Moreover, the expression of CDK2, cyclinD1, P21, MMP2, MMP9, E-cadherin, b-catenin and vimentin was determined by the western blot analysis. Consequently, CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and kept most of the cells in the S phase. The expression of proteins related to the proliferation, invasion and migration of HTR-8/SVneo cells were also changed in accordance with the increase of proliferation, invasion and migration of HTR-8/SVneo cells. In addition, lncRNA CEACAMP8 inhibition decreased the expression of E-cadherin and b-catenin, and increased the vimentin expression to promote the epithelial-mesenchymal transition. And, CEACAMP8 overexpression could reverse the above changes. This study indicated that CEACAMP8 inhibition promoted the proliferation, invasion and migration of HTR-8/SVneo cells and lncRNA CEACAMP8 overexpression reversed.

scholarly journals Induction of the epithelial-mesenchymal transition in the endometrium by chronic endometritis in infertile patients

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249775
Author(s):  
Mitsuaki Ishida ◽  
Akie Takebayashi ◽  
Fuminori Kimura ◽  
Akiko Nakamura ◽  
Jun Kitazawa ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Expression Profiles ◽  
Causative Factor ◽  
Endometrial Biopsy ◽  
Chronic Endometritis ◽  
Mesenchymal Transition ◽  
Infertility Patients ◽  
The Relationship ◽  
Infertile Patients ◽  
E Cadherin

Background The purpose of the present study was to evaluate the relationship between chronic endometritis and the epithelial-mesenchymal transition in the endometrium of infertile patients in the implantation phase. Methods Endometrial biopsy specimens from 66 infertility patients were analyzed. The presence of chronic endometritis was investigated by immunostaining for CD138. Immunohistochemical staining for E-cadherin, N-cadherin, Slug, and Snail was performed, and the expression profiles were statistically analyzed according to the presence of chronic endometritis. When the loss of E-cadherin expression and/or the positive expression of N-cadherin was detected, the specimen was considered epithelial-mesenchymal transition-positive. Epithelial-mesenchymal transition-positive cases were also statistically analyzed according to the presence of chronic endometritis. The characteristics of the patients in the epithelial-mesenchymal transition-positive and epithelial-mesenchymal transition-negative groups were compared. The association between variables, including age, body mass index, gravidity, parity, and each causative factor of infertility and epithelial-mesenchymal transition positivity was analyzed. Results The rates of the loss of E-cadherin expression, the gain of N-cadherin and epithelial-mesenchymal transition positivity were significantly higher in chronic endometritis patients. The expression of Slug, cytoplasmic Snail, and nuclear Snail was also detected at significantly higher rates in chronic endometritis patients. Chronic endometritis were related to the epithelial-mesenchymal transition. Conclusion The epithelial-mesenchymal transition was frequently detected in the endometrium in infertile patients with chronic endometritis. Since the epithelial-mesenchymal transition is associated with chronic endometritis, the epithelial-mesenchymal transition appears to be involved in the alteration of mechanisms of implantation.

scholarly journals Expression and Clinical Utility of Transcription Factors Involved in Epithelial–Mesenchymal Transition during Thyroid Cancer Progression

2021 ◽  
Vol 10 (18) ◽  
pp. 4076
Author(s):  
Enke Baldini ◽  
Chiara Tuccilli ◽  
Daniele Pironi ◽  
Antonio Catania ◽  
Francesco Tartaglia ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Thyroid Cancer ◽  
Cancer Progression ◽  
Clinical Utility ◽  
Epithelial Mesenchymal Transition ◽  
Clinicopathological Parameters ◽  
Mrna Levels ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
E Cadherin

The transcription factors involved in epithelial–mesenchymal transition (EMT-TFs) silence the genes expressed in epithelial cells (e.g., E-cadherin) while inducing those typical of mesenchymal cells (e.g., vimentin). The core set of EMT-TFs comprises Zeb1, Zeb2, Snail1, Snail2, and Twist1. To date, information concerning their expression profile and clinical utility during thyroid cancer (TC) progression is still incomplete. We evaluated the EMT-TF, E-cadherin, and vimentin mRNA levels in 95 papillary TC (PTC) and 12 anaplastic TC (ATC) tissues and correlated them with patients’ clinicopathological parameters. Afterwards, we corroborated our findings by analyzing the data provided by a case study of the TGCA network. Compared with normal tissues, the expression of E-cadherin was found reduced in PTC and more strongly in ATC, while the vimentin expression did not vary. Among the EMT-TFs analyzed, Twist1 seems to exert a prominent role in EMT, being significantly associated with a number of PTC high-risk clinicopathological features and upregulated in ATC. Nonetheless, in the multivariate analysis, none of the EMT-TFs displayed a prognostic value. These data suggest that TC progression is characterized by an incomplete EMT and that Twist1 may represent a valuable therapeutic target warranting further investigation for the treatment of more aggressive thyroid cancers.

scholarly journals Expression and Biological Functions of EPC1 in Nasopharyngeal Carcinoma

2021 ◽  
Vol 24 (11) ◽  
pp. 845-851
Author(s):  
Yongmei Dai ◽  
Wenhan Chen ◽  
Chen Huang ◽  
Shiyin Luo ◽  
Junpeng Huang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Induced Apoptosis ◽  
And Function ◽  
Cancer Tissues ◽  
E Cadherin

Background: Comb homolog enhancer 1 (EPC1) gene is one of the important members of epigenetic inhibitor PCG family. It shows carcinogenic potential in a variety of malignant tumors, but the expression and role of EPC1 in nasopharyngeal carcinoma are unclear. The aim of this study was to explore the expression and function of enhancer of polycomb homolog 1 (EPC1) in nasopharyngeal carcinoma (NPC). Methods: The differential expression of EPC1 in the cancer tissues and cell lines of NPC was examined by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). EPC1 expression, cell proliferation, and apoptosis were detected in NPC cell lines after EPC1 silencing, and the levels of the epithelial-mesenchymal transition (EMT)-related proteins E-cadherin and vimentin were detected in NPC cells after EPC1 silencing. The study was performed at Fujian Provincial Hospital, Fujian, China, from 2018 to 2019. Results: We found that EPC1 was significantly upregulated in the cancer tissues and cell lines of NPC (P<0.001). Furthermore, knockdown of EPC1 inhibited the growth and metastasis of NPC cells. E-cadherin and vimentin were detected in NPC cells after EPC1 was knocked out. It was confirmed that inhibition of EPC1 resulted in increased E-cadherin expression (P<0.001) and decreased vimentin expression (P<0.001), suggesting that inhibition of EPC1 could inhibit the EMT in NPC cells. Conclusion: EPC1 expression was upregulated in NPC tissues and cell lines. Knockout of EPC1 effectively inhibited the growth of NPC cells, induced apoptosis, and inhibited invasion and metastasis. Inhibition of EPC1 could inhibit the EMT in NPC cells. All of the above findings support the viewpoint that EPC1 plays a pro-cancer role in NPC.

scholarly journals The Epithelial-Mesenchymal Transition, E-cadherin and Tumor Progression in Ovarian Serous Tumors

Folia Medica ◽  
2019 ◽  
Vol 61 (2) ◽  
pp. 296-302
Author(s):  
Desislava M. Bozhkova ◽  
Elena G. Poryazova-Markova
Keyword(s):  
Tumor Progression ◽  
Epithelial Mesenchymal Transition ◽  
Ovarian Tumors ◽  
Benign Tumors ◽  
Cell Phenotype ◽  
Ovarian Carcinomas ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Benign Ovarian Tumors ◽  
E Cadherin

Abstract Background: The epithelial-mesenchymal transition (EMT), which is a change in the cell phenotype from epithelial to mesenchymal morphology, is an important step in the invasion process and metastasis of ovarian carcinomas. It is known that the suppression of cell adhesion molecules such as E-cadherin and the expression of mesenchymal markers such as Vimentin are key processes in EMT. There is controversy in the literature about the EMT status of ovarian carcinomas. Aim: To investigate EMT status using immunohistochemical expression of E-cadherin in benign, primary malignant serous ovarian tumors and metastases from them in order to assess their significance in tumor progression. Materials and methods: The study included a retrospective investigation of 217 ovarian epithelial tumors. Ninety-two cases of serous ovarian tumors and metastases were examined for expression of E-cadherin. Results: In our study, the predominant histological subtype in benign ovarian tumors and carcinomas was serous (73% and 61%, respectively). 65% of benign tumors demonstrated EMT negative status. The majority of carcinomas demonstrated EMT positive status (82%), whereas negative EMT status was only observed in 18% of cases. 89% of the metastases showed EMT positive status, whereas only 11% of them showed negative EMT status. In 6 selected cases with positive EMT status we found Vimentin expression in tumor cells. Conclusion: Positive EMT status (reduced E-cadherin expression) is a characteristic of ovarian carcinomas and metastases, but not of benign serous ovarian tumors.

scholarly journals Src SH3/2 Domain-mediated Peripheral Accumulation of Src and Phospho-myosin Is Linked to Deregulation of E-cadherin and the Epithelial-Mesenchymal Transition

2004 ◽  
Vol 15 (6) ◽  
pp. 2794-2803 ◽  
Author(s):  
Egle Avizienyte ◽  
Valerie J. Fincham ◽  
Valerie G. Brunton ◽  
Margaret C. Frame
Keyword(s):  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Cell Contact ◽  
Cell Plasticity ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Dependent Cell ◽  
Adhesion Complex ◽  
E Cadherin ◽  
Cell Cell

Elevated Src kinase in epithelial cancer cells induces adhesion changes that are associated with a mesenchymal-like state. We recently showed that Src induces dynamic integrin adhesions in KM12C colon cancer cells, whereas E-cadherin–dependent cell-cell contacts become disorganized. This promotes a fibroblastic-like morphology and expression of the mesenchymal marker vimentin. Furthermore, Src-induced deregulation of E-cadherin, and the associated mesenchymal transition, is dependent on integrin signaling (Avizienyte et al., Nat. Cell Biol. 2002, 4, 632–638), although the nature of downstream signals that mediate these Src- and integrin-dependent effects are unknown. Here we show that the SH2 and SH3 domains of Src mediate peripheral accumulation of phospho-myosin, leading to integrin adhesion complex assembly, whereas loss of SH2 or SH3 function restores normal regulation of E-cadherin and inhibits vimentin expression. Inhibitors of MEK, ROCK, or MLCK also suppress peripheral accumulation of phospho-myosin and Src-induced formation of integrin-dependent adhesions, whereas at the same time restoring E-cadherin redistribution to regions of cell-cell contact. Our data therefore implicate peripheral phospho-myosin activity as a point of convergence for upstream signals that regulate integrin- and E-cadherin–mediated adhesions. This further implicates spatially regulated contractile force as a determinant of epithelial cell plasticity, particularly in cancer cells that can switch between epithelial and mesenchymal-like states.

Effect of PTPRB on metastasis of colorectal carcinoma and induction of epithelial-mesenchymal transition.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15099-e15099
Author(s):  
Xingyue Weng ◽  
Shu Zheng
Keyword(s):  
Cell Lines ◽  
Protein Tyrosine Phosphatase ◽  
Epithelial Mesenchymal Transition ◽  
Tyrosine Phosphatase ◽  
Multiple Cancer ◽  
Vimentin Expression ◽  
Term Survival ◽  
Mesenchymal Transition ◽  
Protein Tyrosine ◽  
E Cadherin

e15099 Background: Colorectal cancer (CRC) is one of the most common and lethal cancers worldwide. Metastasis and recurrence are believed to be responsible for limiting long-term survival of patients with CRC. Protein tyrosine phosphatase, receptor type B ( PTPRB) belongs to the protein tyrosine phosphatase family. Multiple studies have previously demonstrated that dysregulation of PTPRB function and expression has been shown to correlate with carcinogenesis and tumor progression in multiple cancer types. Methods: In this study, we used CRC cell lines to explore the expression of PTPRB and to analyze the biological function of PTPRB protein. Surgical tumor specimens were collected for immunohistochemical staining to evaluate PTPRB expression.Real-time polymerase chain reaction (PCR) and western blot analysis were used to confirm genes and proteins of interest, respectively. Results: PTPRB is expressed at significantly higher levels in CRC tissues compared to adjacent non-tumor tissues and in CRC cell lines with high metastasis potential. PTPRB knockdown decreased the number of invasive CRC cells in a vitro wound healing model, and also reduced tumor metastasis in vivo. Conversely, PTPRB overexpression decreased E-cadherin expression and promoted vimentin expression, while PTPRB knockdown had the opposite effect. Hypoxic conditions induced EMT and promoted metastasis in CRC cells, but these effects were eliminated by PTPRB knockdown. EMT blockade via TWIST1 knockdown inhibited the migration and invasiveness of CRC cells, and even increased PTPRB expression could not reverse this effect. Conclusions: PTPRB is upregulated in CRC and overexpression of PTPRB promotes the metastasis of CRC. Moreover, our study revealed the effect of PTPRB on promoting EMT, as reflected in increased vimentin and decreased E-cadherin expression. PTPRB is a novel therapeutic target for the treatment of CRC.

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