FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway

Chen, C. H.; Lu, Pengfei; Chen, Y. C.; Fu, Shanlin; Wu, Kou Juey; Tsou, Ann-Ping; Lee, Y. C.G.; Lin, Tai-Du; Hsu, Shih-Lan; Lin, Wey Jinq; Huang, Chi Ying F.; Chou, Chen Kung

doi:10.1038/sj.onc.1210207

Cited by 84 publications

(111 citation statements)

References 29 publications

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“…FLJ10540 has several names, including CEP55 (Fabbro et al, 2005), C10orf3 (Sakai et al, 2006) and URCC6. FLJ10540 is overexpressed in human colon cancer (Sakai et al, 2006), in hepatocellular carcinoma (Chen et al, 2007) and in lung cancer (Chen et al, 2009), suggesting that it may function as an oncogene in tumor development. In addition, we previously showed that the overexpression of FLJ10540 contributes to cellular transformation through the activation of PI3K/AKT (Chen et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…FLJ10540 is overexpressed in human colon cancer (Sakai et al, 2006), in hepatocellular carcinoma (Chen et al, 2007) and in lung cancer (Chen et al, 2009), suggesting that it may function as an oncogene in tumor development. In addition, we previously showed that the overexpression of FLJ10540 contributes to cellular transformation through the activation of PI3K/AKT (Chen et al, 2007). However, no systematic analysis of the FLJ10540 expression and its clinicopathological and functional significance has been carried out for OCSCC.…”

Section: Introductionmentioning

confidence: 99%

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Expression of FLJ10540 is correlated with aggressiveness of oral cavity squamous cell carcinoma by stimulating cell migration and invasion through increased FOXM1 and MMP-2 activity

Chien

et al. 2009

Oncogene

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Matrix metalloproteinase (MMP)-2 plays critical roles in tumor development and in the metastasis of multiple cancers, including human oral cavity squamous cell carcinoma (OCSCC). One of the upstream regulators of MMP-2 is FOXM1, which is overexpressed in a microarray dataset of OCSCC. It is interesting that FLJ10540 exhibits similar gene expression profiles with MMP-2 and FOXM1, raising the possibility that these molecules might participate in MMP-2-elicited cancer progression and metastasis of OCSCC. To examine this connection, we first showed that FLJ10540 was significantly overexpressed in OCSCC. A strong FLJ10540 expression was significantly correlated with an advanced tumor node metastasis stage and the cumulative 5-year survival rate. Thus, an elevated FLJ10540 expression is an indicator of poor survival. Functionally, FLJ10540 had the abilities to stimulate cell migration and invasion in oral cancer cells through increased FOXM1 and MMP-2 expressions. Conversely, the depletion of the FLJ10540 expression by small interefering RNAs suppressed the FOXM1 and MMP-2 protein expressions. The suppression of either FLJ10540 or FOXM1 could cause significant inhibition on cell migratory and invasive ability in oral cancer cells. Finally, the immunohistochemical and western blotting analyses of human aggressive OCSCC specimens showed a significant positive correlation among FLJ10540, FOXM1 and MMP-2 expressions. These findings suggest that FLJ10540 is not only an important prognostic factor but also a new therapeutic target in the FLJ10540/FOXM1/MMP-2 pathway for OCSCC treatment.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression of FLJ10540 is correlated with aggressiveness of oral cavity squamous cell carcinoma by stimulating cell migration and invasion through increased FOXM1 and MMP-2 activity

Chien

et al. 2009

Oncogene

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“…Soon after, overexpression of CEP55 was found in lung adenocarcinoma, gastric carcinoma and hepatocellular carcinoma, where it promote cell proliferation and invasion (17,21,22). It was among the top 70 most highly overexpressed genes in an analysis across 12 cancer types including lung, lymphoma, medulloblastoma and breast, and was identified in prognostic signatures for these cancers (18,23).…”

Section: Discussionmentioning

confidence: 99%

“…Its overexpression and activation was regulated via aberrantly upregulated PI3K/AKT pathways and Forkhead box protein M1 in lung cancer, hepatocellular carcinoma and head-neck squamous cell carcinoma (17,21,25). In glioma, the EGFR and its mutations contributed to tumorigenesis and biology via various ways.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, CEP55 is required for midbody structure and the completion of cytokinesis at the terminal stage (14). Overexpressing of CEP55 Overexpression of centrosomal protein 55 regulates the proliferation of glioma cell and mediates proliferation promoted by EGFRvIII in glioblastoma U251 cells were found in several human tumors and various tumor cell lines (15)(16)(17). However, the relationship between EGFRvIII and CEP55 in proliferation regulation of glioma cells and the effect of CEP55 on these malignant features of GBM is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of centrosomal protein 55 regulates the proliferation of glioma cell and mediates proliferation promoted by EGFRvIII in glioblastoma U251 cells

et al. 2017

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Abstract. The epidermal growth factor receptor (EGFR) is often amplified in glioma, with the most common extracellular domain mutation being EGFR variant III (EGFRvIII). Abnormal EGFRvIII signaling has been shown to be important in driving tumor progression. Centrosomal protein 55 (CEP55), a member of the centrosomal relative proteins family, participates cytokinesis in the cell cycle. It exists in a few normal tissues and various tumor cells. The expression and function of CEP55 in human glioma cells need to investigate. In this study, the expression of CEP55 was detected in 40 cases of glioma tissues and 10 cases of non-tumor brain tissue. The proliferation of glioblastoma U251 cells was analyzed after transfection with EGFRvIII and CEP55 siRNA. We found that the expression of CEP55 was increased significantly in the glioma tissues than in normal brain tissue. The proliferation of U251 cells increased remarkably after transfection with EGFRvIII. Knockdown of CEP55 inhibited proliferation of U251 cells and was able to eliminate the effect of promoting proliferation induced by EGFRvIII in U251 cells. CEP55 played a key role in the proliferation of glioma cells and mediated EGFRvIII-stimulated proliferation in glioma cells. CEP55 might be a novel molecular therapeutic target in patients with gliomas expressing EGFRvIII.

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Synergistic effects of BAY606583 on docetaxel in esophageal cancer through modulation of ERK1/2

Mohammadi

Asadi

Jafari

2022

Cell Biochemistry & Function

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Docetaxel (DTX) is a taxane chemotherapy agent used to treat many types of cancers, including esophageal squamous cell carcinoma. Adenosine is a purinergic signaling molecule that contributes to cancer cell proliferation via A2B adenosine receptor (A2BAR) activation. Extracellular signal‐regulated protein kinase (ERK) plays a crucial role in cell proliferation in various types of cancers. Stimulation of A2BAR involves a regulated ERK signaling pathway, and might provide a fascinating approach for treatment, leading to decreased proliferation in certain tumors that express A2BAR. Recent studies demonstrated that DTX and A2BAR have anticancer effects. The current study was designed to investigate the synergistic effect of the A2BAR agonist (BAY606583) on DTX in inducing antiproliferation effects on esophageal squamous cells carcinoma (ESCCs). The cell viability was assessed using the MTT assay in KYSE‐30 and Ym‐1 cells. In addition, the synergistic effect of DTX on the A2BAR agonist was evaluated. Subsequently, apoptosis was assessed by Annexin‐V and propidium iodide staining, and Bcl‐2, Bax, and ERK1/2 protein‐level expressions were evaluated by Western blot. Use of BAY606583 and cotreatment of DTX and BAY606583 significantly decreased cell proliferation in KYSE‐30 and Ym‐1 cell lines. The use of BAY606583 and cotreatment of DTX with the A2BAR agonist induced apoptosis in KYSE‐30 and Ym‐1 cells. Western blot analysis revealed that the use of the A2BAR agonist and cotreatment of DTX with the A2BAR agonist inhibited the expression of apoptotic regulatory proteins as well as the expression of ERK1/2 proteins. Our findings suggested that use of BAY606583 and cotreatment of BAY606583/DTX have an antiproliferative effect on ESCC cell lines through ERK signaling pathway inhibition. BAY606583 has a synergistic effect on DTX, which could be used as an adjuvant for esophageal cancer therapy.

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FLJ10540-elicited cell transformation is through the activation of PI3-kinase/AKT pathway

Cited by 84 publications

References 29 publications

Expression of FLJ10540 is correlated with aggressiveness of oral cavity squamous cell carcinoma by stimulating cell migration and invasion through increased FOXM1 and MMP-2 activity

Expression of FLJ10540 is correlated with aggressiveness of oral cavity squamous cell carcinoma by stimulating cell migration and invasion through increased FOXM1 and MMP-2 activity

Overexpression of centrosomal protein 55 regulates the proliferation of glioma cell and mediates proliferation promoted by EGFRvIII in glioblastoma U251 cells

Synergistic effects of BAY606583 on docetaxel in esophageal cancer through modulation of ERK1/2

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