Grhl3 induces human epithelial tumor cell migration and invasion via downregulation of E-cadherin

Zhao, Pan; Guo, Sijia; Tu, Zhenzhen; Di, Lijun; Zha, Xiaojun; Zhou, Haisheng; Zhang, Xuejun

doi:10.1093/abbs/gmw001

Cited by 26 publications

(29 citation statements)

References 28 publications

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“…1 were under 0.05. The reason for low CI values of SQUU-B was suggested that the adhesion protein E-cadherin plays an essential role in metastasis, with reduced levels of E-cadherin promoting cell migration and cell invasion (26). The reason for high max CI values of NA was suggested that it has been reported that fibronectin accelerated cell proliferation and adhesion due to the feature of NA cell line as a fibronectin producing cell line (6).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of IC50 levels immediately after treatment with anticancer reagents using a real‑time cell monitoring device

et al. 2019

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A real-time cell-monitoring analysis (RTCA) system was previously developed based on the change in impedance when cells attach and spread in a culture dish coated with a gold microelectrode array. However, the potential applications of this system have not yet been fully demonstrated. The purpose of this study was to test the utility of the RTCA system to determine the cytotoxicity of four anticancer agents in carcinoma cells. The results were compared with those of the conventional WST-8 assay at the endpoint to determine the potential of the RTCA system as a new real-time assay method to evaluate cytotoxicity. iCELLigence was used as the RTCA system in this study. Suspensions of oral squamous cell carcinoma (OSCC) cell lines were seeded (2x10 4 cells/well) onto the E-plate (the culture plate of the iCELLigence system). After 24 h of culture, anticancer agents were added to each well, and changes in electrical impedance (cell index, CI) were recorded for another 72 h of culture. Cell proliferation was detected in real-time by the RTCA device in an automated, high throughput manner. Then, the IC 50 profiles of the four anticancer agents were calculated based on the real-time cell index values. The results indicated that the RTCA system was useful in evaluating cytotoxic reactions immediately after the addition of the anticancer agents as it was able to record the data in real-time. Furthermore, the IC 50 levels measured by the real-time assay were lower than those measured by the endpoint assay. Thus, RTCA systems can be used to evaluate chemotherapeutic agents in cancer cells as well as their side effects in normal cells.

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Section: Discussionmentioning

confidence: 99%

Evaluation of IC50 levels immediately after treatment with anticancer reagents using a real‑time cell monitoring device

et al. 2019

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“…E-cadherin is thought to be a major suppressor of EMT and tumour invasion, EMT being regarded as a primary marker of normal, non-cancerous, differentiated cells. 16,75,76 A reduction in E-cadherin expression has been linked with other changes involved in de-differentiation, oncogenesis and metastasis. 20,77,78 There is a moderate expression in invasive carcinomas without metastases but elevated levels in metastatic deposits: it is reduced or absent in many tumours and a decline in expression induces microRNAs which function as tumour suppressors, limiting invasive, aggressive behaviour.…”

Section: Cadherinmentioning

confidence: 99%

“…20,77,78 There is a moderate expression in invasive carcinomas without metastases but elevated levels in metastatic deposits: it is reduced or absent in many tumours and a decline in expression induces microRNAs which function as tumour suppressors, limiting invasive, aggressive behaviour. 76,79 Conversely N-cadherin is absent or poorly expressed in resting cells and its expression rises during EMT. However, the link between E-cadherin and aggression is not a secure one, since E-cadherin has been found in all of 69 specimens of squamous cell carcinomas, more than half of which exhibited higher than normal levels especially in late stage tumours.…”

Section: Cadherinmentioning

confidence: 99%

Serine protease modulation of Dependence Receptors and EMT protein expression

McNair

Forrest

Vincenten

et al. 2018

Cancer Biology & Therapy

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Expression of the tumour suppressor Deleted in Colorectal Cancer (DCC) and the related protein neogenin is reduced by the mammalian serine protease chymotrypsin or the bacterial serine protease subtilisin, with increased cell migration. The present work examines whether these actions are associated with changes in the expression of cadherins, β-catenin and vimentin, established markers of the Epithelial-Mesenchymal Transition (EMT) which has been linked with cell migration and tumour metastasis. The results confirm the depletion of DCC and neogenin and show that chymotrypsin and subtilisin also reduce expression of β-catenin in acutely prepared tissue sections but not in human mammary adenocarcinoma MCF-7 or MDA-MB-231 cells cultured in normal media, or primary normal human breast cells. A loss of β-catenin was also seen in low serum media but transfecting cells with a dcc-containing plasmid induced resistance. E-cadherin was not consistently affected but vimentin was induced by low serum-containing media and was increased by serine proteases in MCF-7 and MDA-MB-231 cells in parallel with increased wound closure. Vimentin might contribute to the promotion of cell migration. The results suggest that changes in EMT proteins depend on the cells or tissues concerned and do not parallel the expression of DCC and neogenin. The increased cell migration induced by serine proteases is not consistently associated with the expression of the EMT proteins implying either that the increased migration may be independent of EMT or supporting the view that EMT is not itself consistently related to migration. (241).

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“…Epithelial (E-) cadherin is present in various epithelial cells and tumor cells (19); it is a fundamental component of the adherens junctions (the cytoplasmic connection between neighboring cells) and is known to mediate aggregation-dependent cell survival (20). Loss of E-cadherin gene expression in carcinoma cells may lead to increased cell apoptosis, cell death, cell invasion and metastasis (21,22).…”

Section: Introductionmentioning

confidence: 99%

Mast cell chymase affects the proliferation and metastasis of lung carcinoma cells in vitro

Jiang

Hardie

et al. 2017

Oncology Letters

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Abstract. Metastasis of lung carcinoma cells is a major cause of organ failure and mortality of patients with lung cancer. Lung mast cells are a type of immune cell which reside in the respiratory mucosa. High numbers of mast cells are associated with the majority of common types of cancer; however, the effects of mast cells on cancer remain unclear. In the present study, the effects of mast cell chymase (MCC) on the proliferation and adhesion of the lung carcinoma cell lines A549 and H520 was investigated. After 24 h of treatment, the highest dose of MCC (50 mU/ml) decreased the proliferation rate of A549 and H520 cells, whereas the lowest dose of MCC (5 mU/ml) resulted in a small increase in the viability. A549 cells treated with MCC lost adhesion ability in a MCC dose-dependent manner; however, these detached cells were able to regrow when transferred to a fresh culture. The protein expression of epithelial (E-) cadherin, p53 and p21 in A549 lung carcinoma cells were detected by western blot analysis. The results of the present study revealed that, following 24 h of treatment, the expression level of E-cadherin was decreased, the p53 tumor suppressor protein was expressed in limited quantities and the expression of p21 was decreased. Zymography was used to examine the effects of MCC on the expression and activation of matrix metalloproteinase-9 (MMP-9) in A549 and H520 cells. The expression of MMP-9 in the two cell lines was time-and MCC dose-dependent. The results of the present study demonstrated that MCC stimulated lung carcinoma cell proliferation and adhesion, as well as regulated E-cadherin expression and the cell cycle, all of which are associated with cancer metastasis. Therefore, MCC may be a potential candidate for lung carcinoma therapy.

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Grhl3 induces human epithelial tumor cell migration and invasion via downregulation of E-cadherin

Cited by 26 publications

References 28 publications

Evaluation of IC50 levels immediately after treatment with anticancer reagents using a real‑time cell monitoring device

Evaluation of IC50 levels immediately after treatment with anticancer reagents using a real‑time cell monitoring device

Serine protease modulation of Dependence Receptors and EMT protein expression

Mast cell chymase affects the proliferation and metastasis of lung carcinoma cells in vitro

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