COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway in human bladder cancer cells

Choi, Eunmi; Kwak, Sahng‐June; Kim, Young‐Myeong; Ha, Kwon‐Soo; Kim, Jong‐Il; Lee, Sam W.; Han, Jeong A.

doi:10.1038/emm.2005.27

Cited by 29 publications

(23 citation statements)

References 23 publications

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“…In support of our model regarding the role of AKT in MCF10A/COX-2 cells, COX-2 expression also inhibits anoikis in bladder cancer cells in a PI3K/AKT dependent manner [22]. In conclusion, our study indicates an important role of COX-2 in early stages of breast cancer progression, suggesting early prevention strategies using COX-2 inhibitors.…”

Section: Discussionsupporting

confidence: 53%

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Cyclooxygenase-2 Expression Induces Genomic Instability in MCF10A Breast Epithelial Cells

Singh

Vincent²,

Berry³

et al. 2007

Journal of Surgical Research

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Section: Discussionsupporting

confidence: 53%

“…The CHK1 protein needs to be in the nucleus to participate in the DNA-damage response signaling mediated by ATM/ ATR. Since COX-2 is known to activate the PI3K/AKT pathway [10,22], we propose that the mechanism of genomic instability in MCF10A/COX-2 cells involves the phosphorylation of CHK1 at Ser-280 by AKT.…”

Section: Discussionmentioning

confidence: 98%

Cyclooxygenase-2 Expression Induces Genomic Instability in MCF10A Breast Epithelial Cells

Singh

Vincent²,

Berry³

et al. 2007

Journal of Surgical Research

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“…Recent studies demonstrated that selective COX-2 inhibitors (including NS-398) which can inhibit cell proliferation or induce apoptosis are found not only in HCC cell lines but also in colorectal [2,3] , esophageal [14] , bladder [15] , prostatic [16] , lung [17] , cervix [18] carcinoma cells. Over-expression of COX-2 has been demonstrated in patients with HCC and high COX-2 expression in non-tumor liver tissue is significantly associated with inflammator y activity [6,8,19] .…”

Section: Discussionmentioning

confidence: 99%

“…COX-2 may be a logical therapeutic target in various human cancers including HCC. However, information regarding the mechanisms involved in these effects is scant and sometimes contradictory [12][13][14][15] . In this study, we examined the effects and possible mechanism of NS-398, a selective COX-2 inhibitor in two human hepatoma cell lines, HepG2, and Huh7.…”

Section: Introductionmentioning

confidence: 99%

Selective COX-2 inhibitor, NS-398, suppresses cellular proliferation in human hepatocellular carcinoma cell linesviacell cycle arrest

Baek

Hur²,

Wang³

et al. 2007

WJG

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AIM:To investigate the growth inhibitory mechanism of NS-398, a selective cyclooxygenase-2 (COX-2) inhibitor, in two hepatocellular carcinoma (HCC) cell lines (HepG2 and Huh7). METHODS:HepG2 and Huh7 cells were treated with NS-398. Its effects on cell viability, cell proliferation, cell cycles, and gene expression were respectively evaluated by water-soluble tetrazolium salt (WST-1) assay, 4'-6-diamidino-2-phenylindole (DAPI) staining, f l o w c y t o m e t e r a n a l y s i s , a n d We s t e r n b l o tt i n g , with dimethyl sulfoxide (DMSO) as positive control. RESULTS: NS-398 showed dose-and time-dependent g r o w t h -i n h i b i t o r y e ffe c t s o n t h e t w o

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“…These results indicated that BDNF and TrkB do not rescue these 3 TCC cell lines from anoikis in such culture system. Only one previous study mentioned the ability of anoikis resistance in TCC cells through COX-2 (cyclooxygenase 2) transfection into human bladder cancer cell line EJ, also under poly-HEMA culture conditions (30). Maybe poly-HEMA coated dish is not suitable for anoikis resistance study in TCC cells, and other methodology such as culture dish with ultra-low attachment coated polystyrene surface may be used for further investigation (31).…”

Section: Discussionmentioning

confidence: 99%

BDNF mediated TrkB activation is a survival signal for transitional cell carcinoma cells

Huang

Lai²,

Wu³

et al. 2010

Int J Oncol

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Abstract. Pathologically, >90% of bladder cancer is transitional cell carcinoma (TCC). Previously, brain-derived neurotrophic factor (BDNF) but not tropomyosin-related kinase B (TrkB) was found in normal urothelium. TrkB activation by BDNF has been shown to promote the progression of several cancers, however, the existence and functional roles of both BDNF and TrkB in TCC have not been elucidated. In this study, three human TCC cell lines, BFTC905, TSGH8301, and T24 were used for the investigation. Both BDNF and TrkB but not TrkA or TrkC identified by RT-PCR and Western blotting were found in these cell lines. Immunostaining demonstrated the cytosolic expression of BDNF and TrkB, as well as membranous expression of TrkB in these cells. BDNF released from three cell lines was also detected in culture medium by ELISA. The proliferation of BFTC905 cells was enhanced by recombinant human BDNF (rhBDNF) in vitro, which was associated with increased phospho-TrkB and phospho-ERK levels. In contrast, TrkB-Fc chimeric protein served as BDNF scavenger eliciting cytotoxicity. Addition of rhBDNF in these cell lines cultured in poly-HEMA [Poly(2-hydroxyethyl methacrylate)] coated dishes for 48 h did not confer resistance to anoikis. Increased phospho-Akt expression was observed transiently within an hour after rhBDNF administration but disappeared 24 h later. Weekly injections of 100 ng rhBDNF into the cancer cell-loading site for 6 weeks promoted BFTC905 xenograft growth in SCID mice. Daily injection of 5 μg TrkB-Fc chimeric protein into the tumor 2 weeks after tumor cell implantation delayed tumor growth concomitant with phospho-TrkB suppression in xenografts. These results indicate that BDNF binding to TrkB receptor is a survival signal for TCC cells. Drugs that block BDNF or TrkB may provide a new and potential approach for TCC therapy.

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COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway in human bladder cancer cells

Cited by 29 publications

References 23 publications

Cyclooxygenase-2 Expression Induces Genomic Instability in MCF10A Breast Epithelial Cells

Cyclooxygenase-2 Expression Induces Genomic Instability in MCF10A Breast Epithelial Cells

Selective COX-2 inhibitor, NS-398, suppresses cellular proliferation in human hepatocellular carcinoma cell linesviacell cycle arrest

BDNF mediated TrkB activation is a survival signal for transitional cell carcinoma cells

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