Nitrosative Stress in Rotated Three-Dimensional Colorectal Carcinoma Cell Cultures Induces Microtubule Depolymerization and Apoptosis

Laguinge, Luciana M.; Lin, Shuling; Samara, Raed; Salesiotis, Anastasios N.; Jessup, J. Milburn

doi:10.1158/0008-5472.can-03-3663

Cited by 15 publications

(17 citation statements)

References 16 publications

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“…It should be noted that plated tumor cells may respond to nitrosative stress in a different manner than those undergoing fluid shear stress similar to that expected when malignant cells are traveling through the blood stream, i.e. see for example the studies conducted by Laguinge et al on 3-D rotated colorectal carcinoma cells 121 .…”

Section: S-nitrosylation Inhibition Of Apoptosis In Cancer Cellsmentioning

confidence: 99%

Nitric Oxide and Cancer Development

et al. 2007

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Abstract:The role of nitric oxide (NO) in cancer development has become a very active research area. This review presents an overview of many studies that implicate an important role of NO in the development of cancer. These include results in experimental models as well as many observations made on NO and inducible nitric oxide synthase (iNOS) in human cancers. Our survey of the literature has allowed us to conclude that in general large levels of NO will kill cancer cells but paradoxically at intermediate to lower levels NO prevents cancer cell apoptosis and enhances tumor growth. This basic tenet has been demonstrated in many experimental models. The mechanistic basis of how intermediate levels of NO mediate tumor development is an active area of research and is the subject of this review. NO mediated S-nitrosylation of key enzymes and regulatory proteins plays a critical role. Key proteins S-nitrosylated which enhance tumor development include several caspases involved in apoptosis, PTEN the tumor suppressor protein, Bcl-2 the mitochondrial protein which protects from apoptosis, OGG1 the DNA repair protein and methionine adenosyl transferase the liver protein which synthesizes adenosylmethionine. The S-nitrosylation of these proteins enhances DNA mutations, prevents cancer cell apoptosis and enhances oncogenic cell growth. (J Toxicol Pathol 2007; 20: 77-92)

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Section: S-nitrosylation Inhibition Of Apoptosis In Cancer Cellsmentioning

confidence: 99%

Nitric Oxide and Cancer Development

et al. 2007

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“…Hence, a major test of the potential for cancer cells to metastasize is their ability to survive detachment from their matrix and exposure to culture in suspension under anchorage-independent conditions. MacPherson and Montagnier (4) first showed that this ability to grow under anchorage-independent conditions was a hallmark of transformed or malignant cells, an observation that has been supported by others (5,6), whereas Laguinge (7) showed that the ability of human colorectal cancer (CRC) to survive in suspension culture is directly related to metastatic potential.…”

Section: Introductionmentioning

confidence: 96%

“…Goldberg et al (10) showed that anoikis in a human breast cancer cell line was associated with up-regulation of TRAIL expression. As a result, we postulated that TRAIL and its receptors may be involved in the anoikis that we have observed in suspension cultures of human CRC cells (7). There are four distinct TRAIL receptors, all belonging to the TNFR superfamily: TRAIL-R1 (DR4), TRAIL-R2 (DR5), TRAIL-R3 (TRID/ DcR1/lymphocyte inhibitor of TRAIL), and TRAIL-R4 (DcR2; refs.…”

Section: Introductionmentioning

confidence: 96%

“…Fifty percent to 70% confluent CRC cells were extracted and the lysates were blotted as described in Laguinge (7). The primary antibodies used were a murine IgG monoclonal anti-DR4 antibody (Imgenex), a rabbit IgG polyclonal anti-DR5 antibody (Chemicon), a rabbit IgG polyclonal anticleaved caspase-3 (Asp 175 ) antibody, a rabbit IgG polyclonal anticleaved caspase-8 (Asp 374 ) antibody (Cell Signaling Technology), and a mouse IgG monoclonal anti-h-tubulin antibody (Chemicon).…”

Section: Introductionmentioning

confidence: 99%

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DR5 Receptor Mediates Anoikis in Human Colorectal Carcinoma Cell Lines

Laguinge¹,

Samara²,

Wang

et al. 2008

Cancer Research

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As human colorectal cancer (CRC) cells metastasize to distant sites, they are susceptible to detachment-induced cell death or anoikis -a form of apoptosis that occurs when anchoragedependent CRC cells go into suspension. Our goal was to identify whether tumor necrosis factor receptor apoptosisinducing ligand (TRAIL) receptors mediate anoikis in human CRC cells. First, we assessed whether caspases of the extrinsic (caspase-8) or intrinsic (caspase-9) death pathways were involved. Caspase-8 was cleaved during exposure to suspension culture in four CRC lines, and cell death was inhibited by caspase-3 and caspase-8 inhibitors but not by a caspase-9 inhibitor. Gene transcripts in macrophage inflammatory protein-101 (MIP-110), a weakly metastatic human CRC, were increased at least 2-fold for TRAIL-R2 (DR5) and TRAIL after 24 h of suspension culture compared with cells in monolayer culture. The increased expression of DR5 was confirmed at the protein level at 24 h, and exposure of MIP-101 cells to an antagonistic antibody to DR5 decreased caspase-8 activation. The antagonistic antibody to DR5 inhibited anoikis in four human CRC lines. Treatment with an antagonistic DR4 antibody or a neutralizing antibody to TRAIL ligand did not reduce anoikis consistently. Knockdown of DR5 or TRAIL also inhibited anoikis, whereas exogenous TRAIL or FasL did not consistently increase anoikis. In summary, DR5 receptor mediates death signals for anoikis in human CRC cells through the extrinsic apoptotic pathway. [Cancer Res 2008;68(3):909-17]

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“…Then cells were incubated with a mouse IgG 1 monoclonal anti-CEA that is directed to an N-terminal domain (MN3) antibody ( Immunoblotting. Confluent CRC cells (50-70%) were extracted and the lysates were blotted as described in Laguinge et al (24). The antibodies used were as follows: mouse monoclonal anti-CEA antibody (COL-1, NeoMarkers), rabbit polyclonal anti-pAkt (S Immunoprecipitation.…”

Section: Introductionmentioning

confidence: 99%

Carcinoembryonic Antigen Inhibits Anoikis in Colorectal Carcinoma Cells by Interfering with Trail-R2 (DR5) Signaling

Samara¹,

Laguinge²,

Jessup

2007

Cancer Research

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Carcinoembryonic antigen (CEA) is a tumor marker that is associated with metastasis, poor response to chemotherapy of colorectal cancer (CRC), and anoikis, a form of apoptosis caused by cell detachment from matrix that is dependent on TRAIL-R2 (DR5) and caspase-8 activation in CRC. Although CEA is a homophilic binding protein that may provide survival signals through homotypical cell aggregation, we now report that CEA binds TRAIL-R2 (DR5) directly in twohybrid assays to decrease anoikis through the extrinsic pathway. Deletion of the PELPK sequence (delPELPK) of CEA (delPELPK CEA) restores sensitivity to anoikis while it maintains its cell aggregation function. Wild-type (WT) CEA also increases experimental hepatic metastasis, whereas the delPELPK CEA does not. Thus, membrane CEA interacts with DR5 to inhibit anoikis and increase metastatic potential in CRC. [Cancer Res 2007;67(10):4774-82]

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Nitrosative Stress in Rotated Three-Dimensional Colorectal Carcinoma Cell Cultures Induces Microtubule Depolymerization and Apoptosis

Cited by 15 publications

References 16 publications

Nitric Oxide and Cancer Development

Nitric Oxide and Cancer Development

DR5 Receptor Mediates Anoikis in Human Colorectal Carcinoma Cell Lines

Carcinoembryonic Antigen Inhibits Anoikis in Colorectal Carcinoma Cells by Interfering with Trail-R2 (DR5) Signaling

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