scholarly journals Snail family proteins in cervical squamous carcinoma: Expression and significance

2013 ◽  
Vol 36 (4) ◽  
pp. 223 ◽  
Author(s):  
Weidong Zhao ◽  
Ying Zhou ◽  
Hanjie Xu ◽  
Yong Cheng ◽  
Beihua Kong
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Squamous Carcinoma ◽  
Histological Differentiation ◽  
Mesenchymal Transition ◽  
Node Metastasis ◽  
Nuclear Expression ◽  
Snail Family ◽  
E Cadherin

Purpose: Epithelial-mesenchymal transition (EMT) is crucial for tumor progression and metastasis. Snail family members, including Snail, Slug and Smuc, are the transcription factors that repress E-cadherin expression and induce epithelial-mesenchymal transition in some tumor tissues. In this study, the expression of snail family proteins in cervical squamous cancers was evaluated. Methods: A series of 144 samples, comprising 28 cases of normal cervical tissues and 116 cases of squamous cell carcinoma (SCC), were used for analysis. The expression of Snail, Slug, Smuc, E-cadherin and vimentin was assessed in the tissues by immunohistochemistry and was statistically analyzed by SPSS13.0. Results: The increase in nuclear expression of snail and smuc was associated with down-regulation of E-cadherin and up-regulation of vimentin. The nuclear expression of Snail and Smuc was positively associated with lymph node metastasis of the SCC, and the nuclear expression of Snail was also positively related with histological differentiation. In contrast, tumor size, histological differentiation, lymph node metastasis and stages of the SCC were not associated with the expression of Slug, cytpolasmic Smuc or cytoplasm levels of Snail. Conclusion: Snail and Smuc proteins, but not Slug, may contribute to the onset of EMT in SCC. Inhibiting the expression of Snail and Smuc might be a potential therapeutic target for the treatment of metastasis and invasion of cervical carcinomas.

scholarly journals Association of HIF-1α and NDRG2 expression with EMT in gastric cancer tissues

2019 ◽  
Vol 14 (1) ◽  
pp. 217-223
Author(s):  
Ren-Xiang Wang ◽  
Xia-Wan Ou ◽  
Ma-Fei Kang ◽  
Zu-Ping Zhou
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Hypoxia Inducible Factor ◽  
Mesenchymal Transition ◽  
Node Metastasis ◽  
Significant Difference ◽  
Cancer Tissues ◽  
E Cadherin

AbstractObjectiveThis study aims to investigate the differences in the expression of hypoxia-inducible factor-1α (HIF-1α), N-myc downstream-regulated gene 2 (NDRG2) and epithelial mesenchymal transition (EMT)-related proteins in normal gastric tissues, gastric cancer tissues and lymph node metastasis.MethodsImmunohistochemistry was used to detect the expression of HIF-1α, NDRG2, E-cadherin, Snail and Twist in normal gastric tissues, gastric cancer tissues and lymph node metastasis.ResultsIn normal gastric tissues, HIF-1α was not expressed, NDRG2 was highly expressed. There was a significant between the expression of NDRG2 and Snail, as well as of NDRG2 and Twist. In gastric cancer tissues, there was no statistically difference between the expression of HIF-1α and E-cadherin, NDRG2 and E-cadherin. However, there was a significant difference in expression between the expression of HIF-1α and Snail, HIF-1α and Twist, NDRG2 and Snail, and NDRG2 and Twist. In lymph node metastasis tissues, we show that HIF-1α was highly expressed, while NDRG2 was not, and the difference between the expression of HIF-1α and E-cadherin, HIF-1α and Snail, HIF-1α and Twist was not significant.ConclusionHIF-1α may promote EMT, possibly by inhibiting the expression of NDRG2.

Clinical significance of E-cadherin, β-catenin, vimentin and S100A4 expression in completely resected squamous cell lung carcinoma

2013 ◽  
Vol 66 (11) ◽  
pp. 937-945 ◽  
Author(s):  
Hua Zhang ◽  
Jun Liu ◽  
Dongsheng Yue ◽  
Liuwei Gao ◽  
Daowei Wang ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Prognostic Value ◽  
Squamous Cell Lung Carcinoma ◽  
Histological Differentiation ◽  
Vimentin Expression ◽  
Cell Lung Carcinoma ◽  
Node Metastasis ◽  
S100a4 Expression ◽  
E Cadherin

ObjectiveThe aim of this study was to evaluate the prognostic value of E-cadherin, β-catenin, vimentin and S100A4 expression in a cohort of squamous cell lung carcinoma (SqCC) patients.MethodsTumours from 204 patients with surgically resected SqCC were used for the immunohistochemical analyses of E-cadherin, β-catenin, vimentin and S100A4 expression. Correlations between the expression of these markers and clinicopathological parameters were analysed using the χ2 test. The prognostic value of these markers was evaluated using univariate Kaplan–Meier survival analyses and multivariate Cox proportional hazards model analyses.ResultsSignificant associations between E-cadherin expression and T stage (p=0.040), histological differentiation (p=0.005), lymph node metastasis (p<0.001), and recurrence (p<0.001) were identified. Decreased β-catenin expression was significantly correlated with T stage (p=0.003) and lymph node metastasis (p=0.010). Vimentin expression was associated with histological differentiation (p=0.017) and lymph node metastasis (p=0.001). Moreover, significant correlations were observed between S100A4 expression and lymph node metastasis (p=0.020) and recurrence (p<0.001). In the univariate analyses, high E-cadherin expression was a positive indicator for overall survival (OS) (p<0.001) and disease-free survival (DFS) (p<0.001), whereas high S100A4 or vimentin expression were negative indicators for OS (p<0.001 and p=0.010, respectively) and DFS (p<0.001 and p=0.006, respectively). In the multivariate analyses, E-cadherin and S100A4 expression were independent prognostic factors for OS (HR 0.697, 95% CI 0.524 to 0.926, p=0.013, and HR 1.508, 95% CI 1.122 to 2.027, p=0.007, respectively) and DFS (HR 0.634, 95% CI 0.471 to 0.852, p=0.003, and HR 1.490, 95% CI 1.101 to 2.015, p=0.010, respectively).ConclusionsEffective analysis of E-cadherin and S100A4 expression may allow for the identification of patients who are at a high risk of recurrence and poor prognosis in SqCC.

ASAP1 promotes tumor progression and angiogenesis and independently predicts poor prognosis and lymph node metastasis of gastric cancer

2019 ◽  
Author(s):  
Hongyu Gao ◽  
Ling Qin ◽  
Huawen Shi ◽  
Hongfeng Zhang ◽  
Chunfeng Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Epithelial Mesenchymal Transition ◽  
The Cancer Genome Atlas ◽  
Mesenchymal Transition ◽  
Node Metastasis ◽  
Tumor Cell Motility

Abstract Background: Although ArfGAP with SH3 Domain, Ankyrin Repeat and PH Domain 1(ASAP1) is involved in the development of various malignancies, its clinical significance and mechanism in gastric cancer (GC) remains unclear.Methods: The effects of ASAP1 on tumor progression, angiogenesis, and epithelial-mesenchymal transition were evaluated in vitro. The effects of ASAP1 on tumor growth and angiogenesis were also explored in vivo. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to gather ASAP1 expression data.Results: It showed that ASAP1 expression strongly correlated with the TNM stage (P < 0.0001) and lymph node metastasis (P < 0.0001). Multivariate analyses indicated that ASAP1 overexpression (P < 0.0001) was an independent predictor for overall survival in patients with GC. Moreover, the results revealed that ASAP1 overexpression was independently related to lymph node metastasis (P = 0.0001). ASAP1 knockdown inhibited tumor cell motility, migration, invasion, and angiogenesis, which was accompanied with the downregulation of metastatic and angiogenic biomarkers. Furthermore, ASAP1 inhibition resulted in the simultaneous downregulation of mesenchymal markers and upregulation of epithelial markers. In addition, ASAP1 promoted tumor growth and angiogenesis in the xenograft mice model. The combined datasets (TCGA and GEO) suggested that ASAP1 was associated with malignant behavior of tumor and tumor invasion, metastasis, and angiogenesis.Conclusion: To our knowledge, our study is the first to reveal that ASAP1 promotes tumor progression and angiogenesis, and indicates a prognostic potential in GCs.

scholarly journals NOTCH2 negatively regulates metastasis and epithelial-Mesenchymal transition via TRAF6/AKT in nasopharyngeal carcinoma

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
You Zou ◽  
Rui Yang ◽  
Mao-Ling Huang ◽  
Yong-Gang Kong ◽  
Jian-Fei Sheng ◽  
...  
Keyword(s):  
Lymph Node ◽  
Nasopharyngeal Carcinoma ◽  
Lymph Node Metastasis ◽  
Cervical Lymph Node ◽  
Epithelial Mesenchymal Transition ◽  
Cervical Lymph Node Metastasis ◽  
Gene Set Enrichment Analysis ◽  
Mouse Tumor ◽  
Mesenchymal Transition ◽  
Node Metastasis

Abstract Background Clinically, distant metastasis after primary treatment remains a key problem in nasopharyngeal carcinoma (NPC). Thus, identification of the underlying mechanisms and development of novel therapeutic strategies are urgently needed. NOTCH has been shown to function as a tumor promotor that enhances angiogenesis, cancer invasion and metastasis in NPC. However, the precise roles of the four individual NOTCH receptors and their mechanisms of action are unclear. Methods We used Western blot analysis, immunofluorescence, immunohistochemical analysis, phalloidin staining, mouse tumor metastatic dissemination models, gene set enrichment analysis, immunoprecipitation assays and a series of functional assays to determine the potential role of NOTCH2 in regulating NPC metastasis. Results NOTCH2 expression in the NPC tissues of patients with cervical lymph node metastasis was lower than that of patients without cervical lymph node metastasis. Correspondingly, NOTCH2 expression was low in metastatic and poorly differentiated NPC cells. NOTCH2 expression correlated negatively with survival time in patients with NPC. Suppression of NOTCH2 expression promoted NPC cell metastasis, whereas NOTCH2 overexpression inhibited this process. Furthermore, NOTCH2 attenuated the TRAF6–AKT signaling axis via an interaction between the NOTCH2 intracellular domain (N2ICD) and TRAF6, which inhibited epithelial–mesenchymal transition (EMT) and eventually suppressed NPC metastasis. Conclusions These findings reveal that loss of NOTCH2 activates the TRAF6/AKT axis and promotes metastasis in NPC, suggesting that NOTCH2 may represent a therapeutic target for the treatment of NPC.

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