Lentivirus-mediated knockdown of CEP55 suppresses cell proliferation of breast cancer cells

Wang, Ye; Jin, Tao; Dai, Xueming; Xu, Jianrong

doi:10.5582/bst.2016.01010

Cited by 49 publications

(48 citation statements)

References 26 publications

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“…Its aberrant expression has been proposed as an early event in tumourigenesis 25 . Increasing evidence shows that CEP55 has an oncogenic role and its overexpression correlates markedly with tumour stage, aggressiveness, and poor prognosis across multiple tumour types, such as gastric carcinoma, breast cancer, and ovarian carcinoma 15, 20, 21, 26 . In this study, CEP55 was detected as overexpressed in PANC cell lines and in patients with PANC.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence shows that CEP55 is overexpressed in premalignant lesions of the colon and in several solid tumours, including human colon cancer, hepatocellular carcinoma, and bladder cancer 17–19 . Importantly, overexpression of CEP55 promoted cell cycle transition in human gastric cancer 15 ; whereas knockdown of CEP55 inhibited cell growth in breast cancer 20 and gastric cancer 15 , decreased cellular motility and invasion in ovarian cancer cells 21 , and induced cell apoptosis in glioma 22 . These results suggested that CEP55 might serve an oncogenic role and could be a potential target for tumour treatment.…”

Section: Introductionmentioning

confidence: 99%

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Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness

Peng

Zhou

Guo

et al. 2017

Sci Rep

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Centrosomal protein 55 (CEP55) is a microtubule-bundling protein that participants in cell mitosis. It is overexpressed in several solid tumours and promotes the growth and invasion of cancer cells. However, the role of CEP55 in pancreatic cancer (PANC) remains unclear. Herein, upregulated expression of CEP55 (associated with poor prognosis) was detected in PANC using quantitative real-time reverse transcription PCR, western blotting, and immunohistochemistry. Cell migration, colony formation, wound-healing, and Transwell matrix penetration assays, revealed that upregulation of CEP55 promoted PANC cells proliferation, migration, and invasion in vitro, whereas knockdown of CEP55 attenuated it. In an in vivo murine model, CEP55 overexpression accelerated PANC cells tumourigenicity, together with upregulation of the protein levels of invasion-related proteins matrix metalloproteinase (MMP)2, MMP9, and proliferation-related protein Cyclin D1. Downregulation of CEP55 had the reverse effect. Moreover, the nuclear factor κB (NF-κB)/IκBα signalling pathway, which was activated in CEP55-transduced PANC cells and inhibited in CEP55-silenced PANC cells, contributed to CEP55-mediated PANC cell aggressiveness. This study provided new insights into the oncogenic roles of CEP55 and the mechanism by which the NF-κB pathway is hyperactivated in patients with PANC, indicating that CEP55 is a valuable prognostic factor and a potential therapeutic target in PANC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness

Peng

Zhou

Guo

et al. 2017

Sci Rep

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“…2e). Several studies have demonstrated that TPX2 and CEP55 are critical molecules for breast cancer migration, invasion, cell proliferation, and metastasis414243. CDCA5 has been reported to play a crucial role in human lung carcinogenesis and has the potential of being a therapeutic target for oral squamous cell carcinoma4445.…”

Section: Case Study and Discussionmentioning

confidence: 99%

BCIP: a gene-centered platform for identifying potential regulatory genes in breast cancer

Chen

et al. 2017

Sci Rep

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Breast cancer is a disease with high heterogeneity. Many issues on tumorigenesis and progression are still elusive. It is critical to identify genes that play important roles in the progression of tumors, especially for tumors with poor prognosis such as basal-like breast cancer and tumors in very young women. To facilitate the identification of potential regulatory or driver genes, we present the Breast Cancer Integrative Platform (BCIP, http://omics.bmi.ac.cn/bcancer/). BCIP maintains multi-omics data selected with strict quality control and processed with uniform normalization methods, including gene expression profiles from 9,005 tumor and 376 normal tissue samples, copy number variation information from 3,035 tumor samples, microRNA-target interactions, co-expressed genes, KEGG pathways, and mammary tissue-specific gene functional networks. This platform provides a user-friendly interface integrating comprehensive and flexible analysis tools on differential gene expression, copy number variation, and survival analysis. The prominent characteristic of BCIP is that users can perform analysis by customizing subgroups with single or combined clinical features, including subtypes, histological grades, pathologic stages, metastasis status, lymph node status, ER/PR/HER2 status, TP53 mutation status, menopause status, age, tumor size, therapy responses, and prognosis. BCIP will help to identify regulatory or driver genes and candidate biomarkers for further research in breast cancer.

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“…CEP55 (centrosomal protein 55 kDa) is a coiled-coil protein localized to the centrosome in interphase cells and is involved in the mid-body formation during cytokinesis (Fabbro et al, 2005). Over-expression of CEP55 enhances cell cycle progression, whereas knockdown of CEP55 inhibits cell proliferation in breast and gastric cancer (Colak et al, 2013;Tao et al, 2014;Wang, Jin, Dai, & Xu, 2016). Furthermore, CEP55 regulates the phosphoinositide 3-kinase (PI3K)/AKT pathway (Chen et al, 2009;Hwang et al, 2013), presumably leading to the promotion of tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, CEP55 regulates the phosphoinositide 3-kinase (PI3K)/AKT pathway (Chen et al, 2009;Hwang et al, 2013), presumably leading to the promotion of tumorigenesis. Over-expression of CEP55 enhances cell cycle progression, whereas knockdown of CEP55 inhibits cell proliferation in breast and gastric cancer (Colak et al, 2013;Tao et al, 2014;Wang, Jin, Dai, & Xu, 2016). It is thought that aberrant expression of CEP55 is associated with tumorigenesis; however, the developmental function of CEP55 in vertebrates is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Involvement of the centrosomal protein 55 (cep55) gene in zebrafish head formation

et al. 2019

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Mammalian CEP55 (centrosomal protein 55 kDa) is a coiled‐coil protein localized to the centrosome in interphase cells and is required for cytokinesis. A homozygous non‐sense mutation in human CEP55 has been recently identified in perinatal lethal MARCH (multinucleated neurons, anhydramnios, renal dysplasia, cerebellar hypoplasia and hydranencephaly) syndrome. We have isolated zebrafish cep55 mutants defective in head morphology. The zebrafish cep55 gene was expressed in the head including the retina and the pectoral fin at 1 day post‐fertilization (dpf), and extensive cell death was widely observed in the head and tail of the cep55 mutant. In the cep55 mutant, the anterior–posterior distance of the ventral pharyngeal arches was short, and retinal lamination was disorganized. Neural cells, such as islet1‐positive cells and pax2‐positive cells, and fli1b‐positive vascular cells were reduced in the head of the cep55 mutant. Thus, we propose that the zebrafish cep55 mutant is a model organism for human MARCH syndrome.

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Lentivirus-mediated knockdown of CEP55 suppresses cell proliferation of breast cancer cells

Cited by 49 publications

References 26 publications

Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness

Centrosomal protein 55 activates NF-κB signalling and promotes pancreatic cancer cells aggressiveness

BCIP: a gene-centered platform for identifying potential regulatory genes in breast cancer

Involvement of the centrosomal protein 55 (cep55) gene in zebrafish head formation

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