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MicroRNA-21 plays an oncogenic role by targeting FOXO1 and activating the PI3K/AKT pathway in diffuse large B-cell lymphoma
DC Field | Value | Language |
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dc.contributor.author | Go, Heounjeong | - |
dc.contributor.author | Jang, Ji-Young | - |
dc.contributor.author | Kim, Pil-Jong | - |
dc.contributor.author | Kim, Young-Goo | - |
dc.contributor.author | Nam, Soo Jeong | - |
dc.contributor.author | Paik, Jin Ho | - |
dc.contributor.author | Kim, Tae Min | - |
dc.contributor.author | Heo, Dae Seog | - |
dc.contributor.author | Kim, Chul-Woo | - |
dc.contributor.author | Jeon, Yoon Kyung | - |
dc.date.accessioned | 2023-05-08T00:43:28Z | - |
dc.date.available | 2023-05-08T00:43:28Z | - |
dc.date.created | 2018-10-17 | - |
dc.date.created | 2018-10-17 | - |
dc.date.issued | 2015-06 | - |
dc.identifier.citation | Oncotarget, Vol.6 No.17, pp.15035-15049 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | https://hdl.handle.net/10371/192000 | - |
dc.description.abstract | The prognostic implications of miR-21, miR-17-92 and miR-155 were evaluated in diffuse large B-cell lymphoma (DLBCL) patients, and novel mechanism by which miR-21 contributes to the oncogenesis of DLBCL by regulating FOXO1 and PI3K/AKT/mTOR pathway was investigated. The expressions of miR-21, miR-17-92 and miR-155 measured by quantitative reverse-transcription-PCR were significantly up-regulated in DLBCL tissues (n=200) compared to control tonsils (P=0.012, P=0.001 and P<0.0001). Overexpression of miR-21 and miR-17-92 was significantly associated with shorter progression-free survival (P=0.003 and P=0.014) and overall survival (P=0.004 and P=0.012). High miR-21 was an independent prognostic factor in DLBCL patients treated with rituximab-combined chemotherapy. MiR-21 level was inversely correlated with the levels of FOXO1 and PTEN in DLBCL cell lines. Reporter-gene assay showed that miR-21 directly targeted and suppressed the FOXO1 expression, and subsequently inhibited Bim transcription in DLBCL cells. MiR-21 also down-regulated PTEN expression and consequently activated the PI3K/AKT/ mTOR pathway, which further decreased FOXO1 expression. Moreover, miR-21 inhibitor suppressed the expression and activity of MDR1, thereby sensitizing DLBCL cells to doxorubicin. These data demonstrated that miR-21 plays an important oncogenic role in DLBCL by modulating the PI3K/AKT/mTOR/FOXO1 pathway at multiple levels resulting in strong prognostic implication. Therefore, targeting miR-21 may have therapeutic relevance in DLBCL. | - |
dc.language | 영어 | - |
dc.publisher | Impact Journals | - |
dc.title | MicroRNA-21 plays an oncogenic role by targeting FOXO1 and activating the PI3K/AKT pathway in diffuse large B-cell lymphoma | - |
dc.type | Article | - |
dc.identifier.doi | 10.18632/oncotarget.3729 | - |
dc.citation.journaltitle | Oncotarget | - |
dc.identifier.wosid | 000359010700031 | - |
dc.identifier.scopusid | 2-s2.0-84934278912 | - |
dc.citation.endpage | 15049 | - |
dc.citation.number | 17 | - |
dc.citation.startpage | 15035 | - |
dc.citation.volume | 6 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Kim, Pil-Jong | - |
dc.contributor.affiliatedAuthor | Paik, Jin Ho | - |
dc.contributor.affiliatedAuthor | Heo, Dae Seog | - |
dc.contributor.affiliatedAuthor | Kim, Chul-Woo | - |
dc.contributor.affiliatedAuthor | Jeon, Yoon Kyung | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | TRANSCRIPTION FACTORS | - |
dc.subject.keywordPlus | MALIGNANT-LYMPHOMA | - |
dc.subject.keywordPlus | TUMOR-SUPPRESSOR | - |
dc.subject.keywordPlus | P-GLYCOPROTEIN | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PATHOGENESIS | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | AKT | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | SIGNATURES | - |
dc.subject.keywordAuthor | diffuse large B-cell lymphoma | - |
dc.subject.keywordAuthor | miR-21 | - |
dc.subject.keywordAuthor | miR-17-92 cluster | - |
dc.subject.keywordAuthor | miR-155 | - |
dc.subject.keywordAuthor | FOXO1 | - |
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