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dc.contributor.authorSo Yong Lee
dc.contributor.authorJin Suk Cho
dc.contributor.authorDong Yeon Yuk
dc.contributor.authorDong Cheul Moon
dc.contributor.authorJae Kyung Jung
dc.contributor.authorHwan Soo Yoo
dc.contributor.authorYoung Moon Lee
dc.contributor.authorSang Bae Han
dc.contributor.authorKi-Wan Oh
dc.contributor.authorJin Tae Hong
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea
dc.contributor.otherCollege of Pharmacy and CBITRC, Chungbuk National University, 48, Gaesin-dong, Heungduk-gu, Cheongju, Chungbuk, 361-763, South Korea; Corresponding author. jinthong@chungbuk.ac.kr
dc.date.accessioned2025-10-09T04:54:49Z
dc.date.available2025-10-09T04:54:49Z
dc.date.issued01-01-2009
dc.identifier.urihttp://www.sciencedirect.com/science/article/pii/S1347861319311119
dc.identifier.urihttp://digilib.fisipol.ugm.ac.id/repo/handle/15717717/40834
dc.description.abstractNuclear transcription factor-κB (NF-κB) is constitutively activated in prostate and colon cancers and is related with the resistance of cancer cells against chemotherapeutics. Previously, we found that obovatol, an active compound isolated from Magnolia obovata, inhibited cancer cell growth through inhibition of NF-κB activity. We investigated here whether obovatol could sensitize cancer cells against docetaxel through inhibition of NF-κB activity in prostate cancer (LNCaP and PC-3) and colon cancer (SW620 and HCT116) cells. The combination treatment with each drug at one half the respective IC50 dose (5 μM obovatol + 5 nM docetaxel) was more effective and significant (60% – 70%) in the inhibition of cancer cell growth than single treatment by each drug (20% – 40%); inhibition was exerted through a significant increase of apoptosis induction (60% – 80%) by the combination treatment compared to the single treatment (10% – 30%). Correlating well with the synergistic inhibition (combination indices are less than 1 in all cell types), the combination significantly inhibited NF-κB activities as well as expression of NF-κB target apoptotic cell death proteins, but decreased anti-apoptotic cell death proteins. Similar combination effects of obovatol with other chemotherapeutic agents (paclitaxel, cisplatin, and doxorubicin) on the inhibition of cell growth and NF-κB activity were also found. These results indicate that obovatol augments cell growth inhibition by chemotherapeutics through inactivation of NF-κB and suggest that obovatol may have therapeutic advantages in the combination treatment with other chemotherapeutics.[Supplementary Figure: available only at http://dx.doi.org/10.1254/jphs.09048FP] Keywords:: obovatol, docetaxel, combination treatment, nuclear transcription factor-κB (NF-κB), apoptotic cell death
dc.language.isoEN
dc.publisherElsevier
dc.subject.lccTherapeutics. Pharmacology
dc.titleObovatol Enhances Docetaxel-Induced Prostate and Colon Cancer Cell Death Through Inactivation of Nuclear Transcription Factor-κB
dc.typeArticle
dc.description.pages124-136
dc.description.doi10.1254/jphs.09048FP
dc.title.journalJournal of Pharmacological Sciences
dc.identifier.oaioai:doaj.org/journal:1d72ad15c4c54237a45dbc67e5504066
dc.journal.infoVolume 111, Issue 2


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