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    ASIA unversity > 資訊學院 > 光電與通訊學系 > 期刊論文 >  Item 310904400/112383

    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/112383

    Title: Curcumin Promotes Connexin 43 Degradation and Temozolomide-Induced Apoptosis in Glioblastoma Cells.
    Authors: Bor-Ren Huang;Chon-Haw Tsai;Chun-Chuan Chen;Tzong-Der Way;Jung-Yie Kao;Yu-Shu Liu;Hsiao-Yun Lin;Sheng-Wei Lai;Dah-Yuu Lu
    Contributors: 光電與通訊學系
    Date: 2019-04
    Issue Date: 2019-11-08 10:50:08 (UTC+8)
    Abstract: Glioblastoma (GBM) is the most commonly occurring tumor in the cerebral hemispheres. Currently, temozolomide (TMZ), an alkylating agent that induces DNA strand breaks, is considered the frontline chemotherapeutic agent for GBM. Despite its frontline status, GBM patients commonly exhibit resistance to TMZ treatment. We have recently established and characterized TMZ-resistant human glioma cells. The aim of this study is to investigate whether curcumin modulates cell apoptosis through the alternation of the connexin 43 (Cx43) protein level in TMZ-resistant GBM. Overexpression of Cx43, but not ATP-binding cassette transporters (ABC transporters), was observed (approximately 2.2-fold) in TMZ-resistant GBM cells compared to the Cx43 levels in parental GBM cells. Furthermore, at a concentration of 10μM, curcumin significantly reduced Cx43 protein expression by about 40%. In addition, curcumin did not affect the expression of other connexins like Cx26 or epithelial-to-mesenchymal transition (EMT) proteins such as β-catenin or αE-catenin. Curcumin treatment led to an increase in TMZ-induced cell apoptosis from 4% to 8%. Importantly, it did not affect the mRNA expression level of Cx43. Concomitant treatment with the translation inhibitor cycloheximide (CHX) exerted additional effects on Cx43 degradation. Treatment with the autophagy inhibitor 3-MA (methyladenine) did not affect the curcumin-induced Cx43 degradation. Interestingly, treatment with the proteasome inhibitor MG132 (carbobenzoxy-Leu-Leu-leucinal) significantly negated the curcumin-induced Cx43 degradation, which suggests that curcumin-induced Cx43 degradation occurs through the ubiquitin-proteasome pathway.
    Appears in Collections:[光電與通訊學系] 期刊論文

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