Inhibition of Inhibitor of Nuclear Factor-κB Phosphorylation Increases the Efficacy of Paclitaxel in 
 in Vitro
 and 
 in Vivo
 Ovarian Cancer Models

Mabuchi, Seiji; Ohmichi, Masahide; Nishio, Yukihiro; Hayasaka, Tadashi; Kimura, Akiko; Ohta, Tsuyoshi; Koyama, Jun; Takahashi, Kazuhiro; Yada-Hashimoto, Namiko; Seino-Noda, Hozumi; Sakata, Masahiro; Motoyama, Teiichi; Kurachi, Hirohisa; Testa, Joseph R.; Tasaka, Keiichi; Murata, Yuji

doi:10.1158/1078-0432.ccr-04-0958

Cited by 162 publications

(146 citation statements)

References 51 publications

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“…In relation to these data, PS-341 has been administrated alone or in combination to other drugs in multiple myeloma patients, refractory to conventional therapies [19]. Similar results obtained with other NF-kB inhibitors have been described in ovarian cancer [20], in acute myeloid leukemia [8], and in other neoplasia. In line with these data, we have shown that NF-kB inhibition may be a strategy to increase sensitivity to Etoposide-induced apoptosis in a cell line derived from a CML blast crisis.…”

Section: Discussionmentioning

confidence: 59%

NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

et al. 2006

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Section: Discussionmentioning

confidence: 59%

NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

et al. 2006

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“…Although the molecular basis of resistance to Taxol is not well-documented, mounting evidence supports the role of intrinsically or constitutively activated nuclear factor-κB (NF-κB) in affording protection against programmed cell death. Constitutive high levels of NF-κB activity have been detected in response to chemotherapy and radiation in ovarian cancer (3)(4)(5), pancreatic cancer (6), breast cancer (7,8), and prostate cancer (9). Our recent work has revealed that nuclear RelA and cytoplasmic pI-κBα are significantly associated with a poor prognosis in cancer (10).…”

Section: Introductionmentioning

confidence: 98%

Nuclear Factor-κB Inhibition by Parthenolide Potentiates the Efficacy of Taxol in Non–Small Cell Lung Cancer In vitro and In vivo

Zhang

Qiu²,

Jin³

et al. 2009

Molecular Cancer Research

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In this study, we have examined the molecular events induced by parthenolide, a sesquiterpene lactone, and explored possible mechanisms of resistance and sensitization of tumor cells to Taxol. We showed that parthenolide could antagonize Taxol-mediated nuclear factor-κB (NF-κB) nuclear translocation and activation and Bcl-xl up-regulation by selectively targeting I-κB kinase activity. In A549 cells, inhibition of nuclear factor-κB by parthenolide resulted in activation of the mitochondrial death pathway to promote cytochrome c release and caspase 3 and 9 activation. In contrast, Taxol alone induced apoptosis via a pathway independent of mitochondria cytochrome c cascade. In addition, depletion of Bcl-xl rescued the apoptotic response to Taxol. Moreover, treatment with parthenolide increased the efficacy of the Taxol-induced inhibition of A549 tumor xenografts in mice. This study elucidated the cellular responses induced by parthenolide that decrease the threshold of mitochodriadependent apoptosis in the treatment of non-small cell lung cancer cells.

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“…The chemotherapeutic agent cisplatin (cis-diamminedichloroplatinum; cisPt), widely employed for treatment of human cancer, is a potent inducer of growth arrest and/or apoptosis in most cell types. Anti-invasive properties of cisPt associated with decrease in MMP-2 activity have been reported [3][4][5] with the underlying mechanisms still being poorly understood. Anyway, as regards to that several signalling transduction pathways that can be activated by cisPt treatment, such as mitogen activated protein kinase (MAPK) pathway components, have been correlated to MMPs activation and expression [6,7].…”

Section: Introductionmentioning

confidence: 99%

Effects of cisplatin on matrix metalloproteinase-2 in transformed thyroid cells

Urso

Muscella

Calabriso

et al. 2010

Biochemical Pharmacology

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We investigated the effects of cisplatin (cisPt) on matrix metalloproteinase-2 (MMP-2) gelatinolitic activity in transformed PC E1Araf rat thyroid cells. Cells incubated with increasing cisPt concentrations showed dose-and time-dependent decrease of the MMP-2 protein and activity. CisPt provoked the translocation from the cytosol to the plasma membrane of atypical protein kinase C-zeta (PKC-δ) and the activation of PKB/AKT. The effect of cisPt on MMP-2 was dependent on PKC-δ activation since it was potentiated by a myristoylated PKC-δ pseudo substrate peptide or by PKC-δ down regulation by siRNA. Moreover, MMP-2 activity modulation by cisPt was also dependent on PKB/AKT activation since it was decreased by PKB/AKT down regulation by siRNA or by pharmacological inhibition of PI3K, thus indicating the importance of the balance of PKB/AKT and PKC-δ in regulating the cisPt effect on MMP-2 activity. The PC E1Araf cells displayed a migratory capacity that was blocked by MMP-2 down regulation using siRNA or pharmacological inhibition. The inhibition of cell migration was also obtained with cisPt; in cisPt-treated cells the administration of MMP-2 active protein was able to restore cell migration capacity. In conclusion, the decrease of MMP-2 secretion after cisPt was allowed by PKB/AKT and counteracted by PKC-δ; the cisPt-provoked inhibition of MMP-2 secretion ended in reduction of cell migration.

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Inhibition of Inhibitor of Nuclear Factor-κB Phosphorylation Increases the Efficacy of Paclitaxel in in Vitro and in Vivo Ovarian Cancer Models

Abstract: We investigated whether inhibition of nuclear factor-B (NF B) increases the efficacy of paclitaxel in in vitro

Cited by 162 publications

References 51 publications

NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

NF‐kB inhibition as a strategy to enhance etoposide‐induced apoptosis in K562 cell line

Nuclear Factor-κB Inhibition by Parthenolide Potentiates the Efficacy of Taxol in Non–Small Cell Lung Cancer In vitro and In vivo

Effects of cisplatin on matrix metalloproteinase-2 in transformed thyroid cells

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