Abstract:
:Hepatitis B virus (HBV) X protein (HBx) and cyclooxygenase-2 (COX-2) are all playing roles in hepatocellular carcinoma (HCC), but the reversing effects of COX-2 inhibitors on the neoplastic features caused by HBx protein is still unclear. To further evaluate the therapeutic potential of celecoxib on HBx mediated transformation, HCC cells transfected with HBx gene were treated with COX-2 selective inhibitor, celecoxib. The amount the main metabolite of COX-2, prostaglandin E2 (PGE2), was determined by using high sensitivity ELISA. Electron microscope and flow cytometry was used to analyze cell apoptosis and cell cycle distribution. RT-PCR and Western blot were used to identify the molecules involved in celecoxib induced cell apoptosis. The results showed that celecoxib inhibited cell growth more significantly and also induced more cell apoptosis in HBx over-expression cells than in control cells. Celecoxib could selectively inhibited COX-2 expression and PGE2 production. Celecoxib also inhibited p(473Ser)Akt, raf and p53 expression, and induced apoptosis by release of cytochrome c and activation of caspase 9, 3, and 6, which were more remarkably in HBx positive cells than in control cells. These results suggest that celecoxib had potent cell growth inhibitory effects on HBx positive HCC cells mainly through inducing more cell apoptosis, and these findings provide a new insight into the anticancer effects of celecoxib against HBx related HCC.
journal_name
Mol Carcinogjournal_title
Molecular carcinogenesisauthors
Xie H,Gao L,Chai N,Song J,Wang J,Song Z,Chen C,Pan Y,Zhao L,Sun S,Wu K,Feitelson MA,Liu J,Fan Ddoi
10.1002/mc.20455subject
Has Abstractpub_date
2009-01-01 00:00:00pages
56-65issue
1eissn
0899-1987issn
1098-2744journal_volume
48pub_type
杂志文章abstract::Estrogen is thought to be an important etiologic agent in endometrial and breast cancers. However, the mechanism or mechanisms by which estrogen acts as a hormonal carcinogen are not well understood. We hypothesize that in response to chronic exposure to estrogens, human endometrial stromal fibroblasts (ESF) produce f...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/(sici)1098-2744(199812)23:4<217::aid-mc4>3
更新日期:1998-12-01 00:00:00
abstract::The levels of the antioxidant enzyme manganese superoxide dismutase (Mn-SOD) are frequently decreased in tumor cells and increased in normal cells upon treatment with ionizing radiation. We studied Mn-SOD at different stages during the neoplastic conversion of radiation-initiated Syrian hamster embryo HDR-3 cells. Mn-...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/(SICI)1098-2744(199612)17:4<175::AID-MC1>3
更新日期:1996-12-01 00:00:00
abstract::C>T substitutions at dipyrimidine sites dominate the melanoma genome. We recently analyzed the exomes of spontaneous and neonatal UVR-induced murine melanomas, noting a dramatic change in the genomic footprint at C>T substitutions in the latter. Here we re-analyzed published exome-wide footprints in human melanomas st...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22623
更新日期:2017-06-01 00:00:00
abstract::Variations in oral bacterial communities have been linked to oral cancer suggesting that the oral microbiome is an etiological factor that can influence oral cancer development. The 4-nitroquinoline 1-oxide (4-NQO)-induced murine oral and esophageal cancer model is frequently used to assess the effects of preventive a...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22972
更新日期:2019-05-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章,评审
doi:10.1002/mc.21863
更新日期:2013-05-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.21879
更新日期:2013-06-01 00:00:00
abstract::Concern exists regarding peroxisome proliferator (PP) xenobiotic exposure because many PPs are potent hepatocarcinogens in rodents. The mechanism of carcinogenicity induced by PPs is atypical compared with those of other hepatocarcinogens in that the former appears to involve alterations in expression of PP-activated ...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/(sici)1098-2744(199912)26:4<226::aid-mc2>3
更新日期:1999-12-01 00:00:00
abstract::FAM134B is an autophagy regulator of endoplasmic reticulum and acts as a cancer suppressor in colon cancer. However, the molecular signaling pathways by which FAM134B interacts within colon carcinogenesis is still unknown. Herein, this study aims to determine the interacting partners of FAM134B for the first time in c...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22871
更新日期:2018-11-01 00:00:00
abstract::Polyamine metabolism is a highly coordinated process that is essential for normal development and neoplastic growth in mammals. Although polyamine metabolism is a validated pathway for prevention of carcinogenesis, the mechanisms by which polyamines elicit their tumorigenic effects are poorly understood. In this study...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22051
更新日期:2014-02-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20048
更新日期:2005-02-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20055
更新日期:2004-12-01 00:00:00
abstract::Here, we have demonstrated that xenobiotic activation of the nuclear receptor (CAR, NR1I3) can result in arresting DNA-damaged human hepatocellular carcinoma Huh7 cells at the G2/M phase. Huh7 cells over-expressing CAR were either treated with dimethyl sulfoxide, the CAR activator TCPOBOP (1,4-bis[2-(3,5-dichloropyrid...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20783
更新日期:2012-02-01 00:00:00
abstract::2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is the most abundant mutagenic heterocyclic amine in cooked foods. Two mouse tumor cell lines, BMT11 and FM3A, were exposed to its proximate form, 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OH-PhIP). Fifty-six subclones of BMT11 and 39 subclones of ...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.2940090203
更新日期:1994-02-01 00:00:00
abstract::We found that caffeine significantly inhibited epidermal growth factor (EGF)- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell transformation in the JB6 mouse epidermal cell line. The tumor promoter-induced cell transformation was also blocked by treatment with an adenosine A1 receptor antagonist, 8-phenylt...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20120
更新日期:2005-09-01 00:00:00
abstract::Our previous study demonstrated that phosphatidylinositol 3-kinase (PI3K) is necessary for epidermal growth factor (EGF)-induced cell transformation in mouse epidermal JB6 cells. Akt and the mammalian target of rapamycin (mTOR) are regarded as PI3K downstream effectors. Therefore, in this study, we investigated the ro...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.10140
更新日期:2003-09-01 00:00:00
abstract::Nuclear factor kappa B (NFkappaB) is a central participant in the metastasis and chemoresistance of colorectal cancer (CRC). However, it is not fully understood to what extent NFkappaB contributes to induction of the metastasis-associated matrix metalloprotease-9 (MMP-9) gene and sensitivity to the commonly used chemo...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20288
更新日期:2007-05-01 00:00:00
abstract::Base excision repair (BER) is critical for the maintenance of genome stability because it repairs at least 20,000 endogenously generated DNA lesions/cell/d. Several enzymes within the BER pathway exhibit sequence context dependency during the excision and DNA synthesis steps of repair. New evidence is emerging that ge...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章,评审
doi:10.1002/mc.20497
更新日期:2009-04-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20393
更新日期:2008-05-01 00:00:00
abstract::Extracellular signal-regulated kinase 1/2 (ERK1/2) constitute a point of convergence for complex signaling events that regulate essential cellular processes, including proliferation and survival. As such, dysregulation of the ERK signaling pathway is prevalent in many cancers. In the case of BRAF-V600E mutant melanoma...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章,评审
doi:10.1002/mc.23047
更新日期:2019-09-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.2940110403
更新日期:1994-12-01 00:00:00
abstract::Thymidylate synthase (TYMS) is involved in the folate metabolism and provision of nucleotides needed for DNA synthesis and repair. Thus, functional genetic variants in TYMS may alter cancer risk. In the study, we evaluated associations of three germline variants (rs2790 A > G, rs16430 6 bp > 0 bp, and rs1059394 C > T)...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22097
更新日期:2015-04-01 00:00:00
abstract::LEC (Long-Evans with a cinnamon-like coat color) rats develop hepatocellular carcinomas (HCCs) spontaneously. We examined mutations of codons 12, 13, and 61 of the Ha-ras, Ki-ras, and N-ras genes in four HCCs by the polymerase chain reaction (PCR)-single-stranded DNA direct sequencing method. No ras gene mutations wer...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.2940040405
更新日期:1991-01-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20047
更新日期:2004-10-01 00:00:00
abstract::To study the possible involvement of DNA damage in cell transformation induced by estrogens, we examined whether DNA adduct formation is elicited in cultured Syrian hamster embryo (SHE) cells treated with estrogens and their derivatives by means of the 32P-postlabeling assay. Morphological transformation of the cells ...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/(SICI)1098-2744(199607)16:3<149::AID-MC5>3
更新日期:1996-07-01 00:00:00
abstract::A decrease in the intracellular concentrations of the transcripts for some tumor suppressor genes has been found during murine lung tumorigenesis; for p15INK4b and p16INK4a, this was due to homozygous deletions. We report here a decrease in the mRNA levels of the mutated in colorectal cancer (Mcc) and adenomatous poly...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:
更新日期:1998-01-01 00:00:00
abstract::In tumor cells that have lost responsiveness to the growth inhibitory effects of transforming growth factor beta (TGFbeta), increased TGFbeta production by the tumor cells often contributes to cancer progression, primarily through paracrine mechanisms. Here we investigated the major components of the activator protein...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20189
更新日期:2006-08-01 00:00:00
abstract::The normal function of excision repair cross complementing group 1 (ERCC1) is essential for maintaining genomic integrity and preventing cellular neoplastic transformation, and multiple studies have reported an association between ERCC1 polymorphisms and increased risk of cancers. To test whether the genetic variants ...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章,随机对照试验
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更新日期:2009-03-01 00:00:00
abstract::To assess systematically whether potentially functional polymorphisms in DNA repair genes influence the clinical behavior of non-small-cell lung cancer (NSCLC), we examined the impact of a comprehensive panel of 218 signal nucleotide polymorphisms (SNP) in 50 candidate DNA repair genes on overall survival of NSCLC in ...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20819
更新日期:2012-07-01 00:00:00
abstract::Heat shock protein 60 (HSP60) overexpresses in various types of cancer, but its expression levels and functions in hepatocellular carcinoma (HCC) are still in dispute. We aim to clarify this issue and examine whether HSP60 could be a therapeutic target for HCC. We found drastically enhanced cell apoptosis and suppress...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22827
更新日期:2018-09-01 00:00:00
abstract::Carcinogenesis is a multistep sequential process of clonal expansion of initiated cells associated with the accumulation of multiple cancer-specific heritable phenotypes. The acquisition of these heritable cancer-specific alterations may be triggered by mutational and/or non-mutational changes in the genome that affec...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.21861
更新日期:2013-04-01 00:00:00