https://scholars.lib.ntu.edu.tw/handle/123456789/452814
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | LING-HUNG WEI | en_US |
dc.contributor.author | Kuo M.-L. | en_US |
dc.contributor.author | CHI-AN CHEN | en_US |
dc.contributor.author | Chou C.-H. | en_US |
dc.contributor.author | WEN-FANG CHENG | en_US |
dc.contributor.author | Chang M.-C. | en_US |
dc.contributor.author | Su J.-L. | en_US |
dc.contributor.author | CHANG-YAO HSIEH | en_US |
dc.creator | Wei L.-H.;Kuo M.-L.;Chi-An Chen;Chou C.-H.;Cheng W.-F.;Chang M.-C.;Su J.-L.;Hsieh C.-Y. | - |
dc.date.accessioned | 2020-01-22T07:50:54Z | - |
dc.date.available | 2020-01-22T07:50:54Z | - |
dc.date.issued | 2001 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/452814 | - |
dc.description.abstract | Interleukin-6 (IL-6), a multifunctional cytokine, has recently been implicated in human cervical cancer, though the mechanism remains elusive. This study demonstrates that the anti-apoptotic protein Mcl-1 and IL-6 was concomitantly expressed in human cervical cancer tissues and cell lines, but not in normal cervix tissues. Upon IL-6 treatment, Mcl-1, but not other Bcl-2 family members, was rapidly up-regulated peaking at 4-8 h in human cervical cancer C33A cells. Supporting this observation, using anti-IL-6 or anti-IL-6 receptor anti-body to interrupt the IL-6 autocrine loop in SiHa cells significantly reduced cellular level of Mcl-1. This study hypothesizes that the expression of Mcl-1 in cervical cancer cells is regulated by IL-6. The matter of which signaling pathways transduced by IL-6 is responsible for the Mcl-1 up-regulation is further investigated herein. Blocking the STAT3 or MAPK pathway with dominant-negative mutant STAT3F or the MEK inhibitor PD98059 failed to inhibit IL-6-mediated Mcl-1 expression. Meanwhile, the IL-6-induced Mcl-1 up-regulation was effectively abolished by treatment with PI 3-K inhibitors, LY294002. Additionally, overexpression of dominant-negative (dn) Akt in C33A cells could inhibit the IL-6-induced increase of Mcl-1. Finally, overexpression of IL-6 in C33A cells caused a markable resistance to apoptosis induced by doxorubicin or cisplatin. Transient transfection of IL-6-overexpressed cells with a mcl-1 antisense vector, leading to the attenuation of their apoptosis-resistant activity. In conclusion, the data herein suggest that IL-6 regulated the mcl-1 expression via a PI 3-K/Akt-dependent pathway that may facilitate the oncogenesis of human cervical cancer by modulating the apoptosis threshold. | en_US |
dc.relation.ispartof | Oncogene | en_US |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | 2 (2 amino 3 methoxyphenyl)chromone; 2 morpholino 8 phenylchromone; cisplatin; doxorubicin; interleukin 6; mitogen activated protein kinase; phosphatidylinositol 3 kinase; protein mcl 1; STAT3 protein; apoptosis; article; autocrine effect; cancer cell culture; carcinogenesis; controlled study; female; genetic transfection; human; human cell; priority journal; protein expression; protein family; signal transduction; uterine cervix cancer; Antineoplastic Agents; Apoptosis; Carcinoma, Squamous Cell; Doxorubicin; Female; Green Fluorescent Proteins; Hela Cells; Humans; Interleukin-6; Luminescent Proteins; Neoplasm Proteins; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; Transfection; Tumor Cells, Cultured; Up-Regulation; Uterine Cervical Neoplasms | - |
dc.title | The anti-apoptotic role of interleukin-6 in human cervical cancer is mediated by up-regulation of Mcl-1 through a PI 3-K/Akt pathway | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1038/sj.onc.1204733 | - |
dc.identifier.scopus | 2-s2.0-0035855625 | - |
dc.relation.pages | 5799-5809 | en_US |
dc.relation.journalvolume | 5799 | en_US |
dc.relation.journalissue | 5809 | en_US |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Oncology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Clinical Medicine | - |
crisitem.author.dept | Oncology | - |
crisitem.author.dept | Surgery-NTUCC | - |
crisitem.author.dept | Obstetrics & Gynecology-NTUH | - |
crisitem.author.dept | Oncology-NTUH | - |
crisitem.author.dept | Obstetrics & Gynecology | - |
crisitem.author.orcid | 0000-0001-8789-0859 | - |
crisitem.author.orcid | 0000-0001-6670-7939 | - |
crisitem.author.orcid | 0000-0002-3282-6304 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Cancer Center (NTUCC) | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 醫學系 |
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