scholarly journals Role of Twist and Podoplanin in Partial Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma

2020 ◽  
Vol 31 (6) ◽  
pp. 623-633
Author(s):  
Larissa Santos Amaral Rolim ◽  
Rodrigo Porpino Mafra ◽  
Hellen Bandeira de Pontes Santos ◽  
Lélia Batista de Souza ◽  
Leão Pereira Pinto
Keyword(s):  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Membrane Expression ◽  
Lower Lip ◽  
Mesenchymal Transition ◽  
Twist Expression ◽  
Dissociated Cells ◽  
Invasion Pattern ◽  
Histological Malignancy

Abstract The aim of this study was to perform a comparative analysis of podoplanin (PDPN) and Twist immunoexpressions in lower lip and oral tongue squamous cell carcinomas (LLSCC and OTSCC, respectively). PDPN and Twist immunoexpressions were semi-quantitatively evaluated by analyzing the invasion front, the compressive areas, the large islands and nests and dissociated cells of the chosen carcinomas. Their statistical associations and correlations with clinical-pathological characteristics were verified by the Mann-Whitney and Spearman’s test. Twist expression was low in both carcinomas, with <25% labeling on the invasive front. Significant differences were observed for LLSCC (p=0.032) and OTSCC (p=0.025) regarding PDPN immunoexpression in relation to the worst invasion patterns determined by a histological malignancy gradation system. Statistically significant negative correlations between PDPN membrane expression and general (r=-0.356, p=0.024) and cytoplasmic Twist expressions (r=-0.336; p=0.034) in LLSCC were also observed. Twist and PDPN are suggested to be associated to a more aggressive invasion pattern in both LLSCC and OTSCC cases but not related to the different biological behaviors on these anatomical sites. Also, it was seen that PDPN membrane expression is inversely related to general and cytoplasmic Twist expression in LLSCC cases.

PLK1 Promotes Invasion of Esophageal Squamous Cell Carcinoma Cells through Inducing Epithelial-Mesenchymal Transition

2014 ◽  
Vol 998-999 ◽  
pp. 279-282 ◽  
Author(s):  
Ji Yu Ju ◽  
Wen Jing Yu ◽  
Chun Ling Zhao
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Mrna Level ◽  
Mesenchymal Transition ◽  
Stable Transfectants ◽  
Tumorigenesis And Progression

PLK1 has been implicated in tumorigenesis and progression. The role of PLK1 in carcinogenesis has not been fully understood. In our study, we established PLK1-overexpressed stable transfectants in esophageal squamous cell carcinoma (ESCC) cells. Ectopic overexpression of PLK1 enhanced invasiveness of ESCC cells. Compared with the empty vector-transfected cells, PLK overexpression dramatically decreased expression of E-cadherin and increased expression of Vimentin in ESCC cells. Furthermore, Vimentin was also significantly increased at mRNA level in PLK overexpressed ESCC cells. These data suggest that PLK1 promotes invasion of ESCC cells by inducing EMT.

Iroquois Homeobox 5 Negatively Regulated by miRNA-147 Promotes the Proliferation, Metastasis, and Invasion by Oral Squamous Cell Carcinoma

2021 ◽  
Vol 17 (6) ◽  
pp. 1098-1108
Author(s):  
Ziyu Zhu ◽  
Jiaxing Gong ◽  
Jianlu Kong ◽  
Ying Qian ◽  
Kejie Lu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Cell Multiplication ◽  
Promoting Effect ◽  
Mesenchymal Transition

Oral squamous cell carcinoma (OSCC) is one of the most common tumors worldwide and has one of the highest mortalities. The progression of OSCC is accompanied by changes in the levels of many genes. Iroquois homeobox 5 (IRX5), a novel protein involved in several embryonic developmental processes, has been found in recent years to play a significant role in regulating the growth of malignant tumors. However, its role and mechanism in OSCC are still unclear. In this study, we used nano-PCR to examine the levels of IRX5 in OSCC tissues. Through overexpression and knockdown experiments, we researched the role of IRX5 in regulating OSCC cell multiplication, metastasis, and epithelial-mesenchymal transition (EMT). The results demonstrated that IRX5 expression is higher in OSCC tissues in contrast to adjacent tissues. Overexpression of IRX5 promotes the multiplication, metastasis, invasion, and EMT of OSCC cells. Additional bioinformatics analysis showed that miRNA-147 can target the 3’UTR end of IRX5 and negatively regulate its expression, and overexpression of miRNA-147 can weaken the cancer-promoting effect of IRX5. In conclusion, this study found that IRX5 plays a role in promoting cancer in OSCC, and IRX5 is also negatively regulated by miRNA-147.

547 THE ROLE OF HEAT SHOCK PROTEIN 90 IN HYPOXIA INDUCED ANGIOGENESIS AND EPITHELIAL-MESENCHYMAL TRANSITION OF ESOPHAGEAL SQUAMOUS CELL CANCER

2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Ching Tzao ◽  
Chin-Kun Wang
Keyword(s):  
Cell Migration ◽  
Heat Shock ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Squamous Cell Cancer ◽  
Cell Cancer ◽  
Esophageal Squamous Cell Cancer ◽  
Mesenchymal Transition ◽  
And Migration

Abstract   Hypoxia is known as an important trigger for the development of metastases in human cancers. Heat shock proteins (Hsps) are up-regulated by cellular stressors including hypoxia. To date, the functional role of Hsps within the hypoxic tumor microenvironment for esophageal squamous cell cancer (ESCC) remains poorly defined. Methods CoCl₂ was used to induce hypoxia in cultured ESCC cells which was confirmed by 2′,7′ –dichlorofluorescin diacetate (DCFDA) assay. 7-Dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG), a selective Hsp90 inhibitor, was used to treat 2 ESCC cell lines, KYSE-170 and -510 cells pretreated with or without CoCl₂₂₂₂₂ in different concentrations, followed by cytotoxicity (MTT) and migration assays. In parallel, expression of Hsp90, vascular endothelial growth factor (VEGF), hypoxia-inducible factor-1α (HIF-1α), and markers related to epithelial-mesenchymal transition (EMT) such as snail/E-cadherin, by immunoblot or ELISA while analyzing cell proliferation and migration of treated ESCC cells. Results CoCl₂ induced hypoxia was supported by induction of reactive oxygen species (ROS). CoCl₂ (200 μM) significantly suppressed cell viability and proliferation with a concomitant up-regulation of VEGF and HIF-1α in a dose-dependent fashion. In contrast, cell migration was significantly increased in response to CoCl₂ while down-regulating E-cadherin with a concomitant increase in Snail expression. 17-DMAG decreased expression of VEGF and HIF-1α while inhibiting cell migration and invasion. Conclusion Our data demonstrate that CoCl2 induced hypoxia promotes EMT and angiogensis, which are inhibited by 17-DMAG. These results suggest that hypoxia induced EMT and angiogensis is Hsp90 dependent in ESCC.

The prognostic role of the epithelial-mesenchymal transition markers E-cadherin and Slug in laryngeal squamous cell carcinoma

2015 ◽  
Vol 67 (4) ◽  
pp. 491-500 ◽  
Author(s):  
Rocco Cappellesso ◽  
Gino Marioni ◽  
Marika Crescenzi ◽  
Luciano Giacomelli ◽  
Vincenza Guzzardo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Prognostic Role ◽  
Mesenchymal Transition ◽  
E Cadherin

The role of epithelial-mesenchymal transition in squamous cell carcinoma of the oral cavity

2017 ◽  
Vol 472 (2) ◽  
pp. 237-245 ◽  
Author(s):  
Nina Zidar ◽  
Emanuela Boštjančič ◽  
Marija Malgaj ◽  
Nina Gale ◽  
Tadej Dovšak ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Cavity ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals The Oncogenic Activity of miR-29b-1-5p Induces the Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma

2019 ◽  
Vol 8 (2) ◽  
pp. 273 ◽  
Author(s):  
Miyako Kurihara-Shimomura ◽  
Tomonori Sasahira ◽  
Hiroyuki Shimomura ◽  
Chie Nakashima ◽  
Tadaaki Kirita
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Histological Grade ◽  
Oral Epithelium ◽  
Mesenchymal Transition ◽  
The Relationship

Background: The relationship between miR-29b-1-5p and c-Met proto-oncogene in oral squamous cell carcinoma (OSCC) remains to be investigated. This study aimed to reveal the role of miR-29b-1-5p in the pathogenesis of OSCC using molecular and biological analyses. Methods: We investigated the expression of miR-29b-1-5p, c-Met, and markers of the epithelial-mesenchymal transition (EMT) in the tissues of 49 patients with OSCC and in human OSCC cells with different tumorigenicity. Further, we determined the effects of miR-29b-1-5p on the phenotypes of OSCC cell lines. Results: The expression levels of miR-29b-1-5p in most patients with OSCC were higher than those of the normal oral epithelium. In OSCC, upregulation of miR-29b-1-5p significantly correlated with histological grade, the EMT, and the immunohistochemical grade, indicated by c-Met expression. The prognosis was poor for patients with miR-29b-1-5p expression and coexpression of miR-29b-1-5p and c-Met. In OSCC cells exhibiting the EMT phenotype, knockdown of miR-29b-1-5p suppressed the EMT, which was recovered by enforced expression of c-Met. Further, the mRNA encoding cadherin 1 (CDH1) was a direct target of miR-29b-1-5p. Conclusions: Our results suggest that miR-29b-1-5p acts as an oncogenic miRNA that synergizes with c-Met to induce the EMT of OSCC cells.

scholarly journals Effects of DSPP and MMP20 Silencing on Adhesion, Metastasis, Angiogenesis, and Epithelial-Mesenchymal Transition Proteins in Oral Squamous Cell Carcinoma Cells

2020 ◽  
Vol 21 (13) ◽  
pp. 4734
Author(s):  
Jaya Aseervatham ◽  
Kalu U.E. Ogbureke
Keyword(s):  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Integrin Αvβ3 ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Function Mechanism ◽  
Cancer Cell Adhesion ◽  
Specific Proteins ◽  
E Cadherin

Recent reports highlight the potential tumorigenic role of Dentin Sialophosphoprotein (DSPP) and its cognate partner Matrix Metalloproteinase 20 (MMP-20) in Oral Squamous Cell Carcinomas (OSCCs). However, the function/mechanism of these roles is yet to be fully established. The present study aimed to investigate the effects of DSPP and MMP20 silencing on specific proteins involved in oral cancer cell adhesion, angiogenesis, metastasis, and epithelial-mesenchymal transition (EMT). Stable lines of DSPP/MMP20 silenced OSCC cell line (OSC2), previously established via lentiviral-mediated shRNA transduction, were analyzed for the effects of DSPP, MMP20, and combined DSPP–MMP20 silencing on MMP2, MMP9, integrins αvβ3 and αvβ6, VEGF, Kallikerin- 4,-5,-8,-10, E-cadherin, N-cadherin, Vimentin, met, src, snail, and Twist by Western blot. Results show a significant decrease (p < 0.05) in the expression of MMP2, MMP9, integrin αvβ3, αvβ6, VEGF, Kallikerins -4, -5, -8, -10, N-cadherin, vimentin met, src, snail and twist following DSPP and MMP20 silencing, individually and in combination. On the other hand, the expression of E-cadherin was found to be significantly increased (p < 0.05). These results suggest that the tumorigenic effect of DSPP and MMP20 on OSC2 cells is mediated via the upregulation of the genes involved in invasion, metastasis, angiogenesis, and epithelial-mesenchymal transition (EMT).

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