The transcription factor EGR1 regulates metastatic potential of v-src transformed sarcoma cells

Čermák, Vladimı́r; Kosla, Jan; Plachý, Jiřı́; Trejbalová, Kateřina; Hejnar, Jiřı́; Dvořák, Michal

doi:10.1007/s00018-010-0395-6

Cited by 21 publications

(21 citation statements)

References 47 publications

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“…It has been reported that MYO10 is a target gene of EGR1 in sarcoma cells with metastatic potential (Cermak et al , 2010). Interestingly, the hypothesis that MYO10 is upregulated by EGR1 was recently confirmed by a report that MYO10 was upregulated via an EGR1-dependent pathway in mutant p53 breast tumours (Arjonen et al , 2014).…”

Section: Discussionmentioning

confidence: 99%

Elevated expression of myosin X in tumours contributes to breast cancer aggressiveness and metastasis

Cao

Zhang

et al. 2014

Br J Cancer

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Background:Myosin X (MYO10) was recently reported to promote tumour invasion by transporting integrins to filopodial tips in breast cancer. However, the role of MYO10 in tumours remains poorly defined. Here, we report that MYO10 is required in invadopodia to mediate invasive growth and extracellular matrix degradation, which depends on the binding of MYO10's pleckstrin homology domain to PtdIns(3,4,5)P3.Methods:The expression of MYO10 and its associations with clinicopathological and biological factors were examined in breast cancer cells and breast cancer specimens (n=120). Cell migration and invasion were investigated after the silencing of MYO10. The ability of cells to form invadopodia was studied using a fluorescein isothiocyanate-conjugated gelatin degradation assay. A mouse model was established to study tumour invasive growth and metastasis in vivo.Results:Elevated MYO10 levels were correlated with oestrogen receptor status, progesterone receptor status, poor differentiation, and lymph node metastasis. Silencing MYO10 reduced cell migration and invasion. Invadopodia were responsible for MYO10's role in promoting invasion. Furthermore, decreased invasive growth and lung metastasis were observed in the MYO10-silenced nude mouse model.Conclusions:Our findings suggest that elevated MYO10 expression increases the aggressiveness of breast cancer; this effect is dependent on the involvement of MYO10 in invadopodial formation.

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Section: Discussionmentioning

confidence: 99%

Elevated expression of myosin X in tumours contributes to breast cancer aggressiveness and metastasis

Cao

Zhang

et al. 2014

Br J Cancer

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“…Recently, MYL9 was shown to be necessary for cytoskeletal dynamics and experimental metastasis [9]. For example, MYL9 was regulated by the myocardin-related transcription factor–serum response factor (MRTF-SRF) pathway and was required for tumor cell, megakaryocyte, and tip cell migration in vivo [9–12]; MYL9 overexpression resulted in invasion-promoting functions of cancer-associated fibroblasts [13], and the introduction of exogenous early growth response 1 (EGR1) augmented the metastatic potential of non-metastatic PR9692-E9 cells by activating MYL9[14], while microRNA-10b overexpression or direct knockdown of syndecan-1 increased cancer cell migration and Matrigel invasiveness accompanied by MYL9 upregulation[15]. …”

Section: Introductionmentioning

confidence: 99%

“…Despite much evidence supporting the promoter role of MYL9 in tumor invasion and metastasis [9, 10, 14–16], it has been demonstrated that its clinical significance in human tissues differs by tumor type. In bladder cancer, colon cancer, non–small cell lung cancer, and prostate cancer, total MYL9 expression was downregulated in tumor tissues compared with normal tissues[17–20].…”

Section: Introductionmentioning

confidence: 99%

Expression and prognostic significance of MYL9 in esophageal squamous cell carcinoma

et al. 2017

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ObjectiveMyosin light chain 9 (MYL9) is necessary for cytoskeletal dynamics and experimental metastasis, but its expression in esophageal squamous cell carcinoma (ESCC) has not been addressed. We investigated the expression pattern and clinical significance of MYL9 in patients with ESCC.MethodsWe examined MYL9 expression using quantitative real-time PCR and western blotting in NE1 immortalized esophageal epithelial cells, ESCC cell lines, and paired ESCC tissues. MYL9 protein in 136 primary ESCC tissues and other types of solid tumor was detected using immunohistochemistry. The association between MYL9 expression and clinical parameters and survival was evaluated by statistical analysis.ResultsMYL9 was significantly upregulated in the ESCC cell lines as compared with NE1 cells. In the paired ESCC samples, MYL9 mRNA and protein expression was not significantly different between lesion tissues and the matched adjacent noncancerous tissues. In ESCC tissue, both intratumoral and peritumoral stroma were positive for MYL9. In the 136 ESCC samples, high MYL9 expression in the tumor cells significantly correlated with histological differentiation (p = 0.028), recurrence (p = 0.01), and vital status (p < 0.01). Patients with high MYL9 expression in the tumor cells had poorer overall survival (OS) and recurrence-free survival. Multivariate analysis revealed that high MYL9 expression in tumor cells was an independent and significant risk factor affecting OS after curative treatment (hazard ratio = 2.254, 95% confidence interval = 1.347–3.771, p = 0.002).ConclusionsMYL9 expression might be a promising prognostic marker and therapeutic target in ESCC.

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“…It is involved in the transport of glutamate across the inner mitochondrial membrane (accompanied by H + transportation), which facilitates the malate-aspartate shuttle. The gene has also been validated by another dataset [30]. We hypothesize that the functioning of malate-aspartate shuttle can provide extra energy to cancer cells for gaining the growth advantage against native cells as well as escaping from the original site.…”

Section: Discussionmentioning

confidence: 99%

Computational identification of surrogate genes for prostate cancer phases using machine learning and molecular network analysis

Dong

Liu

2014

Theor Biol Med Model

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BackgroundProstate cancer is one of the most common malignant diseases and is characterized by heterogeneity in the clinical course. To date, there are no efficient morphologic features or genomic biomarkers that can characterize the phenotypes of the cancer, especially with regard to metastasis – the most adverse outcome. Searching for effective surrogate genes out of large quantities of gene expression data is a key to cancer phenotyping and/or understanding molecular mechanisms underlying prostate cancer development.ResultsUsing the maximum relevance minimum redundancy (mRMR) method on microarray data from normal tissues, primary tumors and metastatic tumors, we identifed four genes that can optimally classify samples of different prostate cancer phases. Moreover, we constructed a molecular interaction network with existing bioinformatic resources and co-identifed eight genes on the shortest-paths among the mRMR-identified genes, which are potential co-acting factors of prostate cancer. Functional analyses show that molecular functions involved in cell communication, hormone-receptor mediated signaling, and transcription regulation play important roles in the development of prostate cancer.ConclusionWe conclude that the surrogate genes we have selected compose an effective classifier of prostate cancer phases, which corresponds to a minimum characterization of cancer phenotypes on the molecular level. Along with their molecular interaction partners, it is fairly to assume that these genes may have important roles in prostate cancer development; particularly, the un-reported genes may bring new insights for the understanding of the molecular mechanisms. Thus our results may serve as a candidate gene set for further functional studies.

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The transcription factor EGR1 regulates metastatic potential of v-src transformed sarcoma cells

Cited by 21 publications

References 47 publications

Elevated expression of myosin X in tumours contributes to breast cancer aggressiveness and metastasis

Elevated expression of myosin X in tumours contributes to breast cancer aggressiveness and metastasis

Expression and prognostic significance of MYL9 in esophageal squamous cell carcinoma

Computational identification of surrogate genes for prostate cancer phases using machine learning and molecular network analysis

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