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STAT3 as a Potential Target for Tumor Suppressive Effects of 15-Deoxy-Delta(12,14)-prostaglandin J(2) in Triple Negative Breast Cancer
DC Field | Value | Language |
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dc.contributor.author | Kim, Su-Jung | - |
dc.contributor.author | Cho, Nam-Chul | - |
dc.contributor.author | Hahn, Young-Il | - |
dc.contributor.author | Kim, Seong Hoon | - |
dc.contributor.author | Fang, Xizhu | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.date.accessioned | 2023-03-20T08:51:23Z | - |
dc.date.available | 2023-03-20T08:51:23Z | - |
dc.date.created | 2022-01-26 | - |
dc.date.issued | 2021-09 | - |
dc.identifier.citation | 대한암예방학회지, Vol.26 No.3, pp.207-217 | - |
dc.identifier.issn | 2288-3649 | - |
dc.identifier.uri | https://hdl.handle.net/10371/189556 | - |
dc.description.abstract | STAT3 plays a prominent role in proliferation and survival of tumor cells. Thus, STAT3 has been considered to be a prime target for development of anti-cancer therapeutics. The electrophilic cyclopentenone prostaglandin, 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) has been well recognized for its capability to modulate intracellular signaling pathways involved in cancer cell growth and progression. We previously reported that 15d-PGJ(2) had potent cytotoxicity against harvey-ras transformed human mammary epithelial cells through direct interaction with STAT3. In this study, we have attempted to verify the inhibitory effects of 15d-PGJ(2) on STAT3 signaling in human breast tumor cells. The triple negative breast cancer cell lines, MDA-MB-231 and MDA-MB-468 displaying constitutive phosphorylation of STAT3 on the tyrosine 705 (Tyr705) residue, underwent apoptosis upon inhibition of STAT3 by 15d-PGJ(2). In contrast, estrogen receptor positive MCF-7 breast cancer cells that do not exhibit elevated STAT3 phosphorylation were much less susceptible to 15d-PGJ(2)-induced apoptosis as assessed by PARP cleavage. Furthermore, 15d-PGJ(2) inhibited interleukin-6-induced tyrosine phosphorylation of STAT3 in LNCaP cells. According to molecular docking studies, 15d-PGJ(2) may preferentially bind to the cysteine 259 residue (Cys259) present in the coiled-coil domain of STAT3. Site-directed mutagenesis of STAT3 identified Cys259 to be the critical amino acid for the 15d-PGJ(2)-induced apoptosis as well as epithelial-to-mesenchymal transition. Taken together, these findings suggest STAT3 inactivation through direct chemical modification of its Cys259 as a potential therapeutic approach for treatment of triple negative breast cancer treatment. | - |
dc.language | 영어 | - |
dc.publisher | 대한암예방학회 | - |
dc.title | STAT3 as a Potential Target for Tumor Suppressive Effects of 15-Deoxy-Delta(12,14)-prostaglandin J(2) in Triple Negative Breast Cancer | - |
dc.type | Article | - |
dc.citation.journaltitle | 대한암예방학회지 | - |
dc.identifier.wosid | 000706710600003 | - |
dc.citation.endpage | 217 | - |
dc.citation.number | 3 | - |
dc.citation.startpage | 207 | - |
dc.citation.volume | 26 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | ACTIVATED RECEPTOR-GAMMA | - |
dc.subject.keywordPlus | COILED-COIL DOMAIN | - |
dc.subject.keywordPlus | INHIBITS CELL-GROWTH | - |
dc.subject.keywordPlus | IN-VITRO | - |
dc.subject.keywordPlus | DNA-BINDING | - |
dc.subject.keywordPlus | DOWN-REGULATION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | 15D-PGJ(2) | - |
dc.subject.keywordPlus | LIGAND | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordAuthor | Breast neoplasms | - |
dc.subject.keywordAuthor | Cyclopentenone prostaglandin | - |
dc.subject.keywordAuthor | 15-Deoxy-Delta(12,14)-prostaglandin J(2) | - |
dc.subject.keywordAuthor | STAT3 | - |
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