PMC:3342329 / 4459-6031 JSONTXT

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plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T1550","span":{"begin":1540,"end":1544},"obj":"Protein"},{"id":"T1549","span":{"begin":1408,"end":1412},"obj":"Protein"},{"id":"T1548","span":{"begin":1351,"end":1355},"obj":"Protein"},{"id":"T1547","span":{"begin":613,"end":619},"obj":"Protein"},{"id":"T1546","span":{"begin":607,"end":611},"obj":"Protein"},{"id":"T1545","span":{"begin":601,"end":605},"obj":"Protein"},{"id":"T1544","span":{"begin":578,"end":583},"obj":"Protein"},{"id":"T1543","span":{"begin":539,"end":544},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T2752","span":{"begin":616,"end":619},"obj":"http://www.uniprot.org/uniprot/P04141"},{"id":"T2751","span":{"begin":613,"end":619},"obj":"http://www.uniprot.org/uniprot/P04141"},{"id":"T2750","span":{"begin":601,"end":605},"obj":"http://www.uniprot.org/uniprot/P60568"},{"id":"T2749","span":{"begin":578,"end":583},"obj":"http://www.uniprot.org/uniprot/Q04864"},{"id":"T2748","span":{"begin":539,"end":544},"obj":"http://www.uniprot.org/uniprot/Q04864"},{"id":"T2730","span":{"begin":1540,"end":1544},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T2729","span":{"begin":1351,"end":1355},"obj":"http://www.uniprot.org/uniprot/P51681"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"UBERON-AE","denotations":[{"id":"T1403","span":{"begin":697,"end":703},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T1402","span":{"begin":487,"end":500},"obj":"http://purl.obolibrary.org/obo/UBERON_0002405"},{"id":"T1401","span":{"begin":272,"end":277},"obj":"http://purl.obolibrary.org/obo/UBERON_0001155"},{"id":"T1399","span":{"begin":1451,"end":1455},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"GO-BP","denotations":[{"id":"T1592","span":{"begin":1560,"end":1571},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T1591","span":{"begin":163,"end":174},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T1583","span":{"begin":111,"end":123},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T1581","span":{"begin":1179,"end":1185},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T1580","span":{"begin":926,"end":932},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T1579","span":{"begin":749,"end":755},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T1578","span":{"begin":456,"end":462},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T1569","span":{"begin":921,"end":932},"obj":"http://purl.obolibrary.org/obo/GO_0016049"},{"id":"T1621","span":{"begin":1160,"end":1163},"obj":"http://purl.obolibrary.org/obo/GO_0043880"},{"id":"T1619","span":{"begin":1146,"end":1156},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T1618","span":{"begin":1299,"end":1304},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T1617","span":{"begin":981,"end":986},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T1616","span":{"begin":1294,"end":1304},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T1615","span":{"begin":976,"end":986},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T1614","span":{"begin":832,"end":853},"obj":"http://purl.obolibrary.org/obo/GO_0075136"},{"id":"T1613","span":{"begin":825,"end":853},"obj":"http://purl.obolibrary.org/obo/GO_0052572"},{"id":"T1612","span":{"begin":817,"end":841},"obj":"http://purl.obolibrary.org/obo/GO_0002921"},{"id":"T1611","span":{"begin":817,"end":841},"obj":"http://purl.obolibrary.org/obo/GO_0002920"},{"id":"T1610","span":{"begin":817,"end":841},"obj":"http://purl.obolibrary.org/obo/GO_0006959"},{"id":"T1609","span":{"begin":817,"end":841},"obj":"http://purl.obolibrary.org/obo/GO_0002922"},{"id":"T1607","span":{"begin":404,"end":419},"obj":"http://purl.obolibrary.org/obo/GO_0010467"},{"id":"T1604","span":{"begin":194,"end":213},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T1603","span":{"begin":88,"end":106},"obj":"http://purl.obolibrary.org/obo/GO_0008283"},{"id":"T1602","span":{"begin":49,"end":58},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T1601","span":{"begin":49,"end":58},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T1600","span":{"begin":825,"end":841},"obj":"http://purl.obolibrary.org/obo/GO_0006955"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"GO-MF","denotations":[{"id":"T1669","span":{"begin":1160,"end":1163},"obj":"http://purl.obolibrary.org/obo/GO_0043880"},{"id":"T1668","span":{"begin":607,"end":611},"obj":"http://purl.obolibrary.org/obo/GO_0005135"},{"id":"T1667","span":{"begin":601,"end":605},"obj":"http://purl.obolibrary.org/obo/GO_0005134"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"GO-CC","denotations":[{"id":"T1644","span":{"begin":849,"end":853},"obj":"http://purl.obolibrary.org/obo/GO_0018995"},{"id":"T1642","span":{"begin":1294,"end":1298},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T1641","span":{"begin":976,"end":980},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T1640","span":{"begin":921,"end":925},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T1639","span":{"begin":88,"end":92},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"sentences","denotations":[{"id":"T1425","span":{"begin":426,"end":527},"obj":"Sentence"},{"id":"T1424","span":{"begin":181,"end":425},"obj":"Sentence"},{"id":"T1423","span":{"begin":0,"end":180},"obj":"Sentence"},{"id":"T1430","span":{"begin":1202,"end":1372},"obj":"Sentence"},{"id":"T1429","span":{"begin":1106,"end":1201},"obj":"Sentence"},{"id":"T1428","span":{"begin":860,"end":1105},"obj":"Sentence"},{"id":"T1427","span":{"begin":664,"end":859},"obj":"Sentence"},{"id":"T1426","span":{"begin":528,"end":663},"obj":"Sentence"},{"id":"T1432","span":{"begin":1473,"end":1572},"obj":"Sentence"},{"id":"T1431","span":{"begin":1373,"end":1472},"obj":"Sentence"},{"id":"T32","span":{"begin":0,"end":180},"obj":"Sentence"},{"id":"T33","span":{"begin":181,"end":425},"obj":"Sentence"},{"id":"T34","span":{"begin":426,"end":527},"obj":"Sentence"},{"id":"T35","span":{"begin":528,"end":663},"obj":"Sentence"},{"id":"T36","span":{"begin":664,"end":859},"obj":"Sentence"},{"id":"T37","span":{"begin":860,"end":1105},"obj":"Sentence"},{"id":"T38","span":{"begin":1106,"end":1201},"obj":"Sentence"},{"id":"T39","span":{"begin":1202,"end":1372},"obj":"Sentence"},{"id":"T40","span":{"begin":1373,"end":1472},"obj":"Sentence"},{"id":"T41","span":{"begin":1473,"end":1572},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

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plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T3024","span":{"begin":1499,"end":1509},"obj":"Negative_regulation"},{"id":"T3023","span":{"begin":1540,"end":1544},"obj":"Protein"},{"id":"T3022","span":{"begin":1513,"end":1518},"obj":"Protein"},{"id":"T3021","span":{"begin":1373,"end":1383},"obj":"Positive_regulation"},{"id":"T3020","span":{"begin":1408,"end":1412},"obj":"Protein"},{"id":"T3019","span":{"begin":1387,"end":1392},"obj":"Protein"},{"id":"T3018","span":{"begin":1337,"end":1347},"obj":"Negative_regulation"},{"id":"T3017","span":{"begin":1356,"end":1366},"obj":"Gene_expression"},{"id":"T3016","span":{"begin":1223,"end":1233},"obj":"Binding"},{"id":"T3015","span":{"begin":1351,"end":1355},"obj":"Protein"},{"id":"T3014","span":{"begin":1237,"end":1242},"obj":"Protein"},{"id":"T3013","span":{"begin":1106,"end":1116},"obj":"Positive_regulation"},{"id":"T3012","span":{"begin":1120,"end":1125},"obj":"Protein"},{"id":"T3011","span":{"begin":871,"end":876},"obj":"Protein"},{"id":"T3010","span":{"begin":587,"end":596},"obj":"Positive_regulation"},{"id":"T3009","span":{"begin":587,"end":596},"obj":"Positive_regulation"},{"id":"T3008","span":{"begin":587,"end":596},"obj":"Positive_regulation"},{"id":"T3007","span":{"begin":630,"end":640},"obj":"Gene_expression"},{"id":"T3006","span":{"begin":630,"end":640},"obj":"Gene_expression"},{"id":"T3005","span":{"begin":630,"end":640},"obj":"Gene_expression"},{"id":"T3004","span":{"begin":625,"end":629},"obj":"Protein"},{"id":"T3003","span":{"begin":613,"end":619},"obj":"Protein"},{"id":"T3002","span":{"begin":601,"end":611},"obj":"Protein"},{"id":"T3001","span":{"begin":435,"end":440},"obj":"Protein"},{"id":"T3000","span":{"begin":194,"end":204},"obj":"Positive_regulation"},{"id":"T2999","span":{"begin":208,"end":213},"obj":"Protein"},{"id":"T2998","span":{"begin":0,"end":5},"obj":"Protein"}],"relations":[{"id":"R1921","pred":"themeOf","subj":"T2999","obj":"T3000"},{"id":"R1922","pred":"themeOf","subj":"T3002","obj":"T3005"},{"id":"R1924","pred":"themeOf","subj":"T3003","obj":"T3006"},{"id":"R1925","pred":"themeOf","subj":"T3004","obj":"T3007"},{"id":"R1926","pred":"themeOf","subj":"T3005","obj":"T3008"},{"id":"R1927","pred":"themeOf","subj":"T3006","obj":"T3009"},{"id":"R1928","pred":"themeOf","subj":"T3007","obj":"T3010"},{"id":"R1931","pred":"themeOf","subj":"T3012","obj":"T3013"},{"id":"R1932","pred":"themeOf","subj":"T3014","obj":"T3016"},{"id":"R1933","pred":"themeOf","subj":"T3015","obj":"T3017"},{"id":"R1935","pred":"causeOf","subj":"T3016","obj":"T3018"},{"id":"R1936","pred":"themeOf","subj":"T3017","obj":"T3018"},{"id":"R1937","pred":"themeOf","subj":"T3019","obj":"T3021"},{"id":"R1938","pred":"themeOf","subj":"T3022","obj":"T3024"}],"text":"NF-κB plays a crucial role in the suppression of apoptosis, as well as the induction of cell proliferation and inflammation, and is closely associated with cancer development [26]. Constitutive activation of NF-κB has been described in a great number of cancers including colon cancers, prostate cancers and melanoma [27], and was found to up-regulate anti-apoptotic genes and/or down regulate apoptotic gene expression [28]. Although NF-κB promotes tumor growth, it is required for the immune system to function normally [29]. Studies on c-Rel-deficient mice demonstrated that c-Rel is essential for IL-2, IL-3, GM-CSF, and IFNγ expression in T lymphocytes [30]. C-Rel-deficient mice also have a tissue-specific deficiency of various cytokines and growth factors in T cells and macrophages affecting both innate and humoral immune responses in the host [31]. Therefore, NF-κB can be specially targeted to prevent cancer cell growth by (1) directly affecting apoptotic cancer cell death, (2) stimulating tumor killing lymphocytes infiltration or (3) increasing the production of tumor killing lymphokines. Activation of NF-κB is important in the regulation of CCR-mediated tumor growth and metastasis. It was reported that inhibition of NF-κB by dehydroxymethyl-epoxyquinomicin (DHMEQ) induces cell death of primary effusion lymphoma by inhibition of CCR5 expression [32]. Activation of NF-κB also increases CCL5-mediated oral cancer motility (5) and lung metastasis [33]. Thus, it is possible that inhibition of NF-κB could be involved in CCR5 mediated tumor development."}