Deregulation of Bmi-1 is associated with enhanced migration, invasion and poor prognosis in salivary adenoid cystic carcinoma

Chang, Boyang; Li, Su; He, Qiuming; Z, Liu; Zhao, Luodan; Zhao, Tingting; Wang, Anxun

doi:10.1016/j.bbagen.2014.08.005

Cited by 28 publications

(24 citation statements)

References 31 publications

(38 reference statements)

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“…The literature reports that Bmi-1 expression in bladder tumors, wherein the higher expression of Bmi-1 protein also provided a lower degree of differentiation, increased risk of recurrence and worse prognosis, confirming our results in relation to Bmi-1 expression in poorly differentiated tumors (22). Thus, the Bmi-1 expression is considered a prognostic marker for neoplasias, since the high expression of Bmi-1 is associated with increased tumor invasiveness and the development of metastasis, resulting in more aggressive behavior of tumor cells (12,18). An inverse correlation between E-cadherin and N-cadherin was found in this study, although it was not Table 3.…”

Section: Discussionsupporting

confidence: 77%

“…The literature reports that Bmi-1 is a transcription factor associated with increased aggressiveness and consequently of decreased patient survival rates (17). The overexpression of Bmi-1 was observed to be associated with the induction of EMT, thus promoting the migration, invasion and worse prognosis of tumors (18). Furthermore, as the Bmi-1 marker increases, a decrease of the E-cadherin marker and increase of the N-cadherin marker were observed in neoplastic cells through the correlation analyses.…”

Section: Discussionmentioning

confidence: 99%

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Analysis of the Epithelium-Mesenchymal Transition Process on Oral Squamous Cell Carcinomas

et al. 2017

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The aim of this study is to evaluate the immunohistochemical expression of E-cadherin, N-cadherin and Bmi-1, and their association with clinical parameters and with the degree of histopathological differentiation in oral squamous cell carcinomas. 65 squamous cell carcinoma samples were used for constructing a tissue microarray block, and then immunohistochemistry was performed for different markers. A semi-quantitative analysis of the amount of positive tumor cells was performed by two blind and calibrated observers (Kappa>0.75). The statistical Mann-Whitney and Kruskal-Wallis tests were used to evaluate the data. The correlation between variables was investigated by the Spearman test, and the significance level set at p<0.05. We observed higher expression of Bmi-1 in tumors located in the palate (p<0.0001). In addition, poorly differentiated tumors had a greater amount of Bmi-1 positive cells (p=0.0011). Regarding the other correlations between variables, no significant associations were detected. In conclusion, poorly differentiated squamous cell carcinomas located in the palate have higher immunostaining of Bmi-1, which can characterize activation of the Epithelial-Mesenchymal Transition process in these tumors.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Analysis of the Epithelium-Mesenchymal Transition Process on Oral Squamous Cell Carcinomas

et al. 2017

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“…The sections were incubated with the secondary antibody using a MaxVision™ HRP-Polymer anti-Rabbit IHC Kit (Maixin, Fuzhou, China); colour was developed using a DAB Horseradish Peroxidase Colour Development Kit (Maixin, Fuzhou, China), and the sections were counterstained with haematoxylin. The degree of immunostaining was scored according to both the proportion of positively stained tumour cells and the staining intensity, as described previously [30]. We evaluated HK2 expression by determining the staining index (staining intensity score × proportion of positive tumour cells), which resulted in scores of 0, 1, 2, 3, 4, 6 and 9.…”

Section: Methodsmentioning

confidence: 99%

“…Cell proliferation was evaluated after 24 h using a modified Cell Counting Kit-8 (CCK8) assay (Fanbo, Beijing, China) according to the manufacturer's instructions [30]. The absorbance (optical density, OD) value at 450 nm was determined using a plate reader.…”

Section: Methodsmentioning

confidence: 99%

Hexokinase 2 enhances the metastatic potential of tongue squamous cell carcinoma via the SOD2-H2O2 pathway

Wang

Zhao

et al. 2016

Oncotarget

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The glycolytic enzyme hexokinase (HK2), which is aberrantly expressed in various types of tumours, is associated with metastasis. However, its role in the progression and metastasis of tongue squamous cell carcinoma (TSCC) remains unclear. The results of our study showed that HK2 expression is often deregulated in TSCC patients. Increased HK2 expression was associated with tumour stage, clinical stage, lymph node metastasis, but not pathological grade, and reduced overall survival. Microarray and western blotting analyses revealed increases in HK2 expression in TSCC cells with higher metastatic potential. The following effects were observed with HK2 knockdown: inhibition of cell migration and invasion; reduced SOD2 activity and intracellular H2O2 levels; suppression of pERK1/2, Slug and Vimentin expression; and inhibition of tumour growth and lung metastasis in vivo. Conversely, HK2 overexpression promoted cell migration and invasion, increased SOD2 activity and intracellular H2O2, and enhanced expression of pERK1/2, Slug and Vimentin. Thus, our results demonstrate that deregulation of HK2 expression has an important function in the progression of TSCC and may serve as a biomarker of its metastatic potential in TSCC patients. HK2 enhances the metastatic potential of TSCC by stimulating the SOD2-H2O2 pathway.

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“…EMT is an important mechanism in cancer invasion and metastasis. Many studies have shown that Bmi-1 can regulate EMT in various cancers [26–28], but it is unclear whether Bmi-1 can drive the EMT process in gastric cancer. To explore the role of Bmi-1 in establishing a mesenchymal phenotype in gastric cells, we deleted Bmi-1 using RNA interference (RNAi) (Figure 6A) and examined the expression of the mesenchymal markers fibronectin, vimentin, N-cadherin and SNAIL, as well as the epithelial marker E-cadherin, in AGS cells.…”

Section: Resultsmentioning

confidence: 99%

The SNAIL/miR-128 axis regulated growth, invasion, metastasis, and epithelial-to-mesenchymal transition of gastric cancer

Jiang

Zhang

et al. 2017

Oncotarget

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miR-128 is expressed in various tumors, but its expression and function in gastric cancer have not been defined. Thus, the goal of this study was to characterize miR-128 in gastric cancer. We found first that miR-128 is down-regulated in gastric cancer cell lines and tissues, and this dysregulation is correlated with DNA methylation and the transcription factor SNAIL. Using prediction tools, western blotting, and luciferase reporter assays, we found that Bmi-1 was the direct target of miR-128. Additionally, overexpression of miR-128 inhibited gastric cancer cell migration, invasion, and proliferation by targeting Bmi-1 in vitro and in vivo. We also documented, with receiver operating characteristic curves and Kaplan-Meier survival analysis, that miR-128 and Bmi-1 may be useful markers for diagnosing and estimating the prognosis of gastric cancer patients. As the epithelial-to-mesenchymal transition is an important mechanism associated with cancer invasion and metastasis, we inferred that miR-128 could regulate this mechanism in gastric cancer. In fact, we found that miR-128 could reverse epithelial-to-mesenchymal transition induced by Bmi-1 via the PI3K/AKT pathway. Because SNAIL also acts as a mesenchymal marker, our findings identified a novel positive feedback loop in which the transcription factor SNAIL curbs the expression of miR-128, and then down-regulated miR-128 promotes the expression of Bmi-1; finally, overexpression of Bmi-1 drives the epithelial-to-mesenchymal transition process via the PI3K/AKT pathway, and the expression of SNAIL is up-regulated.

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Deregulation of Bmi-1 is associated with enhanced migration, invasion and poor prognosis in salivary adenoid cystic carcinoma

Cited by 28 publications

References 31 publications

Analysis of the Epithelium-Mesenchymal Transition Process on Oral Squamous Cell Carcinomas

Analysis of the Epithelium-Mesenchymal Transition Process on Oral Squamous Cell Carcinomas

Hexokinase 2 enhances the metastatic potential of tongue squamous cell carcinoma via the SOD2-H2O2 pathway

The SNAIL/miR-128 axis regulated growth, invasion, metastasis, and epithelial-to-mesenchymal transition of gastric cancer

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