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

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.

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Sulfiredoxin may promote metastasis and invasion of cervical squamous cell carcinoma by epithelial–mesenchymal transition

Tumor Biology ◽

10.1177/1010428317695942 ◽

2017 ◽

Vol 39 (3) ◽

pp. 101042831769594

Author(s):

Xiaoyan Chen ◽

Kangyun Lan ◽

Qin Liu ◽

Xue Yang ◽

Hui Wang

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Epithelial Mesenchymal Transition ◽

Cervical Squamous Cell Carcinoma ◽

Expression Level ◽

Migration Activity ◽

Mesenchymal Transition ◽

Siha Cells ◽

E Cadherin

Sulfiredoxin (Srx), a novel oxidative stress-induced antioxidant protein, has been reported to be expressed in several human tumour tissues. However, the expression and functions of Srx in cervical squamous cell carcinoma remain unknown. Here, we proved that expression of Srx was upregulated in cervical tissues as revealed by immunohistochemistry, and revealed a close correlation between the protein’s expression and the expression level of one core epithelial–mesenchymal transition marker, E-cadherin. We demonstrated that Srx was overexpressed in cervical squamous cell carcinoma and its expression level was closely correlated with lymph node metastasis and invasion of cervical squamous cell carcinoma. Meanwhile, Srx expression was negatively correlated with E-cadherin expression. The remission time (tumour-free status after surgery) of the Srx strong staining group was significantly shorter than that of the Srx weak staining group. We silenced Srx by short hairpin RNA in HeLa and SiHa cells. Diminished Srx expression upregulated E-cadherin expression. The cell invasion and migration activity in the ShSrx group were obviously decreased in HeLa and SiHa cells. Moreover, Srx regulated the expression of the other marker of epithelial–mesenchymal transition, vimentin. In conclusion, the study suggested that Srx was highly expressed in cervical squamous cell carcinoma and may promote invasion and metastasis of cervical squamous cell carcinoma via regulating epithelial–mesenchymal transition.

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Knockdown of Snail inhibits epithelial–mesenchymal transition of human laryngeal squamous cell carcinoma Hep-2 cells through the vitamin D receptor signaling pathway

Biochemistry and Cell Biology ◽

10.1139/bcb-2017-0039 ◽

2017 ◽

Vol 95 (6) ◽

pp. 672-678 ◽

Cited By ~ 7

Author(s):

Xue Zhao ◽

Dan Yu ◽

Jingpu Yang ◽

Kai Xue ◽

Yan Liu ◽

...

Keyword(s):

Vitamin D ◽

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Signaling Pathway ◽

Vitamin D Receptor ◽

Squamous Cell ◽

Laryngeal Squamous Cell Carcinoma ◽

Epithelial Mesenchymal Transition ◽

Integrin Subunit ◽

Mesenchymal Transition

It has been well documented that Snail plays a decisive role in various tumors. However, the direct effect of Snail on laryngeal squamous cell carcinoma (LSCC) has not been elaborated. In this study, we firstly detected the expression of Snail in 14 samples of patients with LSCC and found that its content was high in cancer tissues compared with adjacent tissues. Then we established LSCC Hep-2 cells with Snail silencing and validated the knockdown efficiency by Western blotting and real-time PCR. Results showed that silencing of Snail significantly inhibited the ability of adhesion, migration, and invasion of Hep-2 cells. Further study revealed that knockdown of Snail suppressed the epithelial–mesenchymal transition (EMT) process of Hep-2 cells, as evidenced by downregulation of matrix metallopeptidase (MMP)-2, MMP-9, integrin subunit beta 1 (ITGβ1), β-catenin, vimentin, N-cadherin, and fibronectin and upregulation of vitamin D receptor (VDR) and E-cadherin. Additionally, transfection with the small interfering RNA of VDR reversed the effect induced by Snail silencing in Hep-2 cells. Taken together, these results demonstrate that knockdown of Snail can inhibit the EMT process of LSCC cells through the VDR signaling pathway in vitro.

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HPV18 Associated with E-cadherin Expression in Head and Neck Squamous Cell Carcinoma

Revista de Chimie ◽

10.37358/rc.18.10.6596 ◽

2018 ◽

Vol 69 (10) ◽

pp. 2638-2641 ◽

Cited By ~ 1

Author(s):

Simina Boia ◽

Eugen Radu Boia ◽

Raluca Amalia Ceausu ◽

Constantin Nicolae Balica ◽

Ovidiu Alexandru Mederle

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Head And Neck ◽

Squamous Cell ◽

Epithelial Mesenchymal Transition ◽

Neck Squamous Cell Carcinoma ◽

Mesenchymal Transition ◽

Poorly Differentiated ◽

Well Differentiated ◽

E Cadherin

HPV is an important oropharyngeal cancer cause, but it may have a role in other head and neck cancers? HPVpositive head and neck squamous cell carcinoma (HNSCC) epithelial-mesenchymal transition role is unclear. We included 38 cases: 20 laryngeal, 3 corresponding lymph nodes; 5 oropharyngeal, 5 hypopharyngeal, 2 rhynopahryngeal, 2 pharyngolaryngeal and 1 naso-sinusal case. Immunoreactivity was positive in nuclear expression cells, accordingly: score 1 (10-30%), 2 (30-50%) and 3 (]50%). HPV18 immunoexpression appeared in 18 cases (47.36%), (11 laryngeal, 4 oropharyngeal, 1 hypopharyngeal, 1 pharyngolaryngeal and 1 naso-sinusal). The score was 1 in larynx well differentiated type. The score was between 1 and 3 in larynx moderately differentiated types, and a significant correlation HPV18/E-cadherin was found (p=0.031). HPV18+/E-cadherin low values were noticed in larynx, oropharynx, pharyngo-larynx and naso-sinusal well and moderately differentiated types. HPV18-/E-cadherin low values were present in larynx, hypo and rhyno-pharynx moderately and poorly differentiated and larynx well differentiated types. Larynx presented HPV18/E-cadherin and moderately differentiated type significant correlation. Rhyno, hypo-pharyngeal and laryngeal presented HPV18�/E-cadherin low values association for moderately, poorly and undifferentiated types. The oropharyngeal location was associated with E-cadherin maximum values, independently of HPV18 status.

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

Journal of Biomedical Nanotechnology ◽

10.1166/jbn.2021.3085 ◽

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.

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TRPP2 Enhances Metastasis by Regulating Epithelial-Mesenchymal Transition in Laryngeal Squamous Cell Carcinoma

Cellular Physiology and Biochemistry ◽

10.1159/000447914 ◽

2016 ◽

Vol 39 (6) ◽

pp. 2203-2215 ◽

Cited By ~ 17

Author(s):

Kaile Wu ◽

Bing Shen ◽

Feifei Jiang ◽

Lin Xia ◽

Taotao Fan ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Wound Healing ◽

Cell Carcinoma ◽

Squamous Cell ◽

Cell Invasion ◽

Laryngeal Squamous Cell Carcinoma ◽

Epithelial Mesenchymal Transition ◽

Invasion And Metastasis ◽

Mesenchymal Transition ◽

Expression Levels

Background/Aim: Surgery and chemotherapy treatments of human laryngeal squamous cell carcinoma (HLSCC) may fail due to metastasis, in which epithelial-mesenchymal transition (EMT) plays an important role. TRPP2, a nonselective cation channel, is expressed in various cell types and participates in many biological processes. Here, we show that TRPP2 enhanced metastasis by regulating EMT. Methods: We used immunohistochemistry, western blotting, Ca2+ imaging, transwell and wound healing assays to investigate TRPP2 expression levels in HLSCC tissue, and the role of TRPP2 in invasion and metastasis of a human laryngocarcinoma cell line (Hep2 cell). Results: We found that TRPP2 protein expression levels were significantly increased in HLSCC tissue; higher TRPP2 levels were associated with decreased patient survival time and degree of differentiation and advanced clinical stage. Knockdown of TRPP2 by transfection with TRPP2 siRNA markedly suppressed ATP-induced Ca2+ release, wound healing, and cell invasion in Hep2 cells. Moreover, TRPP2 siRNA significantly decreased vimentin expression but increased E-cadherin expression in Hep2 cells. In the EMT signalling pathway, TRPP2 siRNA significantly decreased Smad4, STAT3, SNAIL, SLUG and TWIST expression in Hep2 cells. Conclusion: We revealed a previously unknown function of TRPP2 in cancer development and a TRPP2-dependent mechanism underlying laryngocarcinoma cell invasion and metastasis. Our results suggest that TRPP2 may be used as a biomarker for evaluating patient prognosis and as a novel therapeutic target in HLSCC.

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MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

Bioscience Reports ◽

10.1042/bsr20181882 ◽

2019 ◽

Vol 39 (1) ◽

Cited By ~ 4

Author(s):

Yuan Li ◽

Chenjuan Tao ◽

Lili Dai ◽

Caixia Cui ◽

Chaohui Chen ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Laryngeal Squamous Cell Carcinoma ◽

Critical Role ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

Expression Levels

AbstractIntroduction: Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC.Materials and methods: LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. In vitro cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3′-UTR of SOX4.Results: The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells.Conclusions: Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.

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IQGAP1 silencing suppresses the malignant characteristics of laryngeal squamous cell carcinoma cells

The International Journal of Biological Markers ◽

10.5301/ijbm.5000287 ◽

2017 ◽

Vol 33 (1) ◽

pp. 73-78 ◽

Cited By ~ 2

Author(s):

Xiaoxia Wang ◽

Chun He ◽

Chaohui Li ◽

Benhong Ren ◽

Qing Deng ◽

...

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Epithelial To Mesenchymal Transition ◽

Laryngeal Squamous Cell Carcinoma ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

First Time

Background: Laryngeal squamous cell carcinoma (LSCC) has a poor prognosis due to recurrence and metastasis. IQ-domain GTPase-activating protein 1 (IQGAP1), a scaffold protein, plays an important role in tumorigenesis and malignant development. In this study, we aimed to explore the role of IQGAP1 in LSCC. Methods: Expression of IQGAP1 in human LSCC specimens was assessed by immunohistochemistry. We also evaluated the roles of IQGAP1 in cell proliferation, migration and invasion and epithelial-to-mesenchymal transition (EMT) in Hep-2 cells. Results: The expression of IQGAP1 protein was significantly up-regulated in LSCC tissues compared with normal laryngeal tissues (p = 0.002). Furthermore, the knockdown of IQGAP1 in Hep-2 cells inhibited cell growth, migration and invasion. Moreover, we found that IQGAP1 silencing reversed EMT. Conclusions: These results show for the first time that IQGAP1 is up-regulated in LSCC tissues and plays an important role in LSCC cell proliferation and invasiveness, which indicates that IQGAP1 could work as an oncogene and may serve as a promising molecular target for treatment of LSCC.

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