Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21<sup>WAF1/CIP1</sup> and C/EBPβ expressions and suppressing NF‐κB activation

Hour, Tzyh‐Chyuan; Chen, Jun; Huang, Chao Yuan; Guan, Jian; Lu, Shiu-Hui; Pu, Yeong-Shiau

doi:10.1002/pros.10089

Cited by 125 publications

(72 citation statements)

References 22 publications

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“…Cell cycle control gene cyclindependent kinase inhibitor 1A (p21) was induced >10-fold at 12 hours on curcumin administration. This is supported by a previous study in which curcumin cause G 1 arrest in PC-3 cells by induction of p21 (36). Curcumin has been shown to inhibit cancer cell invasion and metastasis (25,37) by modulating integrin receptors, collagenase activity, and expression of E-cadherin.…”

Section: Curcumin and Global Gene Expression Profiles In Micesupporting

confidence: 77%

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Shen¹,

Hu³

et al. 2006

Molecular Cancer Therapeutics

161

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Curcumin has been shown to prevent and inhibit carcinogeninduced tumorigenesis in different organs of rodent carcinogenesis models. Our objective is to study global gene expression profiles elicited by curcumin in mouse liver and small intestine as well as to identify curcuminregulated nuclear factor E2-related factor 2 (Nrf2) -dependent genes. Wild-type C57BL/6J and Nrf2 knockout C57BL/6J/Nrf2(À/À) mice were given a single oral dose of curcumin at 1,000 mg/kg. Liver and small intestine were collected at 3 and 12 hours after treatments.

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Section: Curcumin and Global Gene Expression Profiles In Micesupporting

confidence: 77%

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Shen¹,

Hu³

et al. 2006

Molecular Cancer Therapeutics

161

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“…Moreover, depending of cell lines tested, curcumin was shown to induce cell cycle arrest in G1 phase in glioma (40) and prostate cancer cells (41,42) or in G2/M phase in colon (17,31,43) and breast cancer cells (14). In our experimental approach, flow cytometry analysis pointed out that curcumin was able to induce cell cycle arrest in G2/M.…”

Section: Discussionmentioning

confidence: 77%

Anti-proliferative potential of curcumin in androgen-dependent prostate cancer cells occurs through modulation of the Wingless signaling pathway

Diederich¹

2011

Int J Oncol

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Abstract. Activation of the Wingless (Wnt)/ß-catenin signaling pathway contributes to prostate tumorigenesis and metastasis. Depending of the stage of prostate cancer development, current drug therapies are of limited efficiency, so that prevention with natural compounds appears as an attractive strategy especially due to the slow progressive development of prostate cancer. We report here that the chemopreventive agent curcumin from the rhizome of Curcuma longa was able to affect cell proliferation of androgen-dependent prostate cancer through the induction of cell cycle arrest in G2 and modulation of Wnt signaling. Curcumin decreases the level of Tcf-4, CBP and p300 proteins implicated in the Wnt transcriptional complex that leads to the decrease of ß-catenin/Tcf-4 transcriptional activity and of the expression of ß-catenin target genes (cyclin D1 and c-myc). Subsequent cell death induction is linked to autophagy. Interestingly, in androgen-independent prostate cancer cells, curcumin does not affect Wnt/ß-catenin transcriptional activity. Altogether our results suggest that curcumin is an interesting chemopreventive agent for early stage prostate cancer.

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“…Prostate cancer cells become more susceptible to cytostatic drug-induced apoptosis when incubated with curcumin. 21 Perhaps, differences between the transformed and nontransformed cells account for these different findings.…”

Section: Discussionmentioning

confidence: 99%

“…11,19,20 Moreover, it has been postulated that NF-kB inhibition increases the susceptibility of various cancers to chemotherapeutic-or radiation-induced apoptosis. 21,22 For instance, the blockade of NF-kB activity in prostate cancer cells inhibits angiogenesis, invasion and metastasis. In human ovarian cancer cells also an inhibition of tumorigenicity could be detected.…”

Section: Introductionmentioning

confidence: 99%

Role of curcumin and the inhibition of NF-κB in the onset of chemotherapy-induced mucosal barrier injury

Land¹,

Blijlevens

Marteijn³

et al. 2003

Leukemia

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The inhibition of nuclear factor kappa B (NF-jB) by, for instance, curcumin is becoming an important new approach in combination with chemotherapy or irradiation for the treatment of a variety of cancers including haematological malignancies. A dose-limiting side effect of anticancer therapy in the gastrointestinal tract is mucosal barrier injury. It is hypothesised that mucosal barrier injury is initiated and amplified by proinflammatory-and NF-jB-regulated mediators. Therefore, the effect of NF-jB inhibition was studied in the onset of mucosal barrier injury. In response to cytostatic drug treatment (arabinoside cytosine (Ara-C) and methotrexate (MTX)), NF-jB was activated in intestinal epithelial cells (IEC-6) resulting in an NF-jB-related induction of tumour necrosis factor alpha and monocyte chemoattractant protein-1. NF-jB inhibition increased the susceptibility of IEC-6 cells to Ara-C as well as MTX-induced cell death when obtained by the addition of caffeic acid phenethyl ester (CAPE), but not using curcumin. In an animal model for MTX-induced mucosal barrier injury, the induction of NF-jB-related cytokines and chemokines was detected upon treatment with MTX. Despite increased susceptibility shown in vitro, the inhibition of NF-jB resulted in a partial amelioration of villous atrophy normally seen in the small intestine upon MTX treatment. These results show that the inhibition of NF-jB does not increase intestinal side effects of the anticancer treatment, suggesting a safe use of curcumin and CAPE in combination with anticancer treatment.

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Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21^WAF1/CIP1 and C/EBPβ expressions and suppressing NF‐κB activation

Abstract: The incorporation of CCM into cytotoxic therapies may be a promising strategy for the treatment of AIPC.

Cited by 125 publications

References 22 publications

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Anti-proliferative potential of curcumin in androgen-dependent prostate cancer cells occurs through modulation of the Wingless signaling pathway

Role of curcumin and the inhibition of NF-κB in the onset of chemotherapy-induced mucosal barrier injury

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Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21WAF1/CIP1 and C/EBPβ expressions and suppressing NF‐κB activation

Abstract: The incorporation of CCM into cytotoxic therapies may be a promising strategy for the treatment of AIPC.

Cited by 125 publications

References 22 publications

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Modulation of nuclear factor E2-related factor 2–mediated gene expression in mice liver and small intestine by cancer chemopreventive agent curcumin

Anti-proliferative potential of curcumin in androgen-dependent prostate cancer cells occurs through modulation of the Wingless signaling pathway

Role of curcumin and the inhibition of NF-κB in the onset of chemotherapy-induced mucosal barrier injury

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Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21^WAF1/CIP1 and C/EBPβ expressions and suppressing NF‐κB activation