Expression of acyl‐CoA synthetase 5 in human endometrium and in endometrioid adenocarcinomas

Gaßler, Nikolaus; Yang, Seung-Ha; Keith, Martina; Helmke, Burkhard; Schirmacher, Peter; Obermüller, Nicholas

doi:10.1111/j.1365-2559.2005.02255.x

Cited by 6 publications

(4 citation statements)

References 18 publications

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“…In addition, they failed to employ in vitro and in vivo experiments to further explore the role of ACS5 in the progression of CRC. Similar to our study, Gassler et al showed that the higher the expression level of ACS5 in endometrial carcinoma, the higher the degree of tumor differentiation [ 22 ]; Gaisa et al reported that the expression level of ACS5 in normal urothelial tissue was significantly higher than that in tumor tissue and reported a gradual loss of ACS5 expression with decreasing cellular differentiation in urothelial cancers [ 23 ]. These two studies suggested that ACS5 was a tumor suppressor, which was contrary to our findings in colorectal cancer, that may be related to the type of tumor.…”

Section: Discussionsupporting

confidence: 89%

Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells

Ding

Tang

Wang

et al. 2017

Canadian Journal of Gastroenterology and Hepatology

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Background and Aims Acyl-CoA synthetase 5 (ACS5) has been reported to be associated with the development of various cancers, but the role of it in colorectal cancer (CRC) is not well understood. The present study aimed to explore the potential role of ACS5 in the development and progression of CRC. Methods ACS5 expression in CRC tissues and CRC cell lines was examined, and its clinical significance was analyzed. The role of ACS5 in cell proliferation, apoptosis, and invasion was examined in vitro. Results We found that ACS5 expression was upregulated in CRC cells and CRC tissues and that high ACS5 expression was more frequent in CRC patients with excess muscular layer and with poor tumor differentiation. Furthermore, knockdown of ACS5 in HT29 and SW480 cells significantly dampened cell proliferation, induced cell apoptosis, and reduced cell migration and invasion. In contrast, the ectopic overexpression of ACS5 in LOVO and SW620 cells remarkably promoted cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion. Enhanced cell growth and invasion ability mediated by the gain of ACS5 expression were associated with downregulation of caspase-3 and E-cadherin and upregulation of survivin and CD44. Conclusions Our data demonstrate that ACS5 can promote the growth and invasion of CRC cells and provide a potential target for CRC gene therapy.

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Section: Discussionsupporting

confidence: 89%

Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells

Ding

Tang

Wang

et al. 2017

Canadian Journal of Gastroenterology and Hepatology

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“…Within the context of tumorogenesis, few reports have been published on ACS5. In adenoma and adenocarcinoma of the small intestine ACS5 expression is decreased [54] while it is up-regulated in gliomas [55], in well-differentiated endometrioid adenocarcinomas [56] and in certain colorectal adenocarcinomas [57]. The RT-qPCR data in our panel of tumors revealed an increase in the expression of ACS5 (p = 0.001), eventhough it has not been confirmed by IHC.…”

Section: Discussionmentioning

confidence: 80%

Gene expression profiling in sinonasal adenocarcinoma

et al. 2009

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BackgroundSinonasal adenocarcinomas are uncommon tumors which develop in the ethmoid sinus after exposure to wood dust. Although the etiology of these tumors is well defined, very little is known about their molecular basis and no diagnostic tool exists for their early detection in high-risk workers.MethodsTo identify genes involved in this disease, we performed gene expression profiling using cancer-dedicated microarrays, on nine matched samples of sinonasal adenocarcinomas and non-tumor sinusal tissue. Microarray results were validated by quantitative RT-PCR and immunohistochemistry on two additional sets of tumors.ResultsAmong the genes with significant differential expression we selected LGALS4, ACS5, CLU, SRI and CCT5 for further exploration. The overexpression of LGALS4, ACS5, SRI, CCT5 and the downregulation of CLU were confirmed by quantitative RT-PCR. Immunohistochemistry was performed for LGALS4 (Galectin 4), ACS5 (Acyl-CoA synthetase) and CLU (Clusterin) proteins: LGALS4 was highly up-regulated, particularly in the most differentiated tumors, while CLU was lost in all tumors. The expression of ACS5, was more heterogeneous and no correlation was observed with the tumor type.ConclusionWithin our microarray study in sinonasal adenocarcinoma we identified two proteins, LGALS4 and CLU, that were significantly differentially expressed in tumors compared to normal tissue. A further evaluation on a new set of tissues, including precancerous stages and low grade tumors, is necessary to evaluate the possibility of using them as diagnostic markers.

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“…ACSL5 expression was variably associated with malignancy, being increased in many colorectal tumors, but decreased in some intestinal tumors including adenocarcinomas (28,29). ACSL5 expression was also increased in well-differentiated, but not poorly-differentiated, endometrial adenocarcinomas (30). ACSL5 mRNA levels were high in primary human gliomas and A172 glioma cells but, in contrast to our findings with ACSVL3, were not detectable in either U87 or U373 glioma cells (31).…”

Section: Discussionmentioning

confidence: 99%

Acyl-CoA Synthetase VL3 Knockdown Inhibits Human Glioma Cell Proliferation and Tumorigenicity

et al. 2009

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The contribution of lipid metabolic pathways to malignancy is poorly understood. Expression of the fatty acyl-CoA synthetase ACSVL3 was found to be markedly elevated in clinical malignant glioma specimens but nearly undetectable in normal glia. ACSVL3 levels correlated with the malignant behavior of human glioma cell lines and glioma cells propagated as xenografts. ACSVL3 expression was induced by the activation of oncogenic receptor tyrosine kinases (RTK) c-Met and epidermal growth factor receptor. Inhibiting c-Met activation with neutralizing anti-hepatocyte growth factor monoclonal antibodies reduced ACSVL3 expression concurrent with tumor growth inhibition in vivo. ACSVL3 expression knockdown using RNA interference, which decreased long-chain fatty acid activation, inhibited anchorage-dependent and anchorageindependent glioma cell growth by ∼70% and ∼90%, respectively. ACSVL3-depleted cells were less tumorigenic than control cells, and subcutaneous xenografts grew ∼60% slower than control tumors. Orthotopic xenografts produced by ACSVL3-depleted cells were 82% to 86% smaller than control xenografts. ACSVL3 knockdown disrupted Akt function as evidenced by RTK-induced transient decreases in total and phosphorylated Akt, as well as glycogen synthase kinase 3β, via a caspase-dependent mechanism. Expressing constitutively active myr-Akt rescued cells from the anchorage-dependent and anchorage-independent growth inhibitory effects of ACSVL3 depletion. These studies show that ACSVL3 maintains oncogenic properties of malignant glioma cells via a mechanism that involves, in part, the regulation of Akt function. [Cancer Res 2009;69(24):9175-82]

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Expression of acyl‐CoA synthetase 5 in human endometrium and in endometrioid adenocarcinomas

Cited by 6 publications

References 18 publications

Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells

Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells

Gene expression profiling in sinonasal adenocarcinoma

Acyl-CoA Synthetase VL3 Knockdown Inhibits Human Glioma Cell Proliferation and Tumorigenicity

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