Resveratrol attenuates the anticancer efficacy of paclitaxel in human breast cancer cells in vitro and in vivo

Fukui, Masayuki; Yamabe, Noriko; Zhu, Bao Ting

doi:10.1016/j.ejca.2010.02.004

Cited by 114 publications

(71 citation statements)

References 43 publications

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“…In agreement with this observation, susceptibility to paclitaxel by breast cancer cells was found to be reduced by antioxidant treatments [21], and resistance to paclitaxel has been associated with the total antioxidant cell capacity in a large series of different cancer cell lines [38], suggesting that oxidative stress contributes to the antineoplastic mechanism of action of this drug. Patients subjected to chemotherapy with paclitaxel present immediate systemic oxidative stress and red blood cell oxidative injury associated with the development of anemia [37].…”

Section: Introductionmentioning

confidence: 78%

TRPA1 and TRPV4 mediate paclitaxel-induced peripheral neuropathy in mice via a glutathione-sensitive mechanism

Materazzi

Fusi

Benemei

et al. 2012

Pflugers Arch - Eur J Physiol

197

188

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Paclitaxel produces a sensory neuropathy, characterized by mechanical and cold hypersensitivity, which are abated by antioxidants. The transient receptor potential vanilloid 4 (TRPV4) channel has been reported to contribute to paclitaxel-evoked allodynia in rodents. We recently showed that TRP ankyrin 1 (TRPA1) channel mediates oxaliplatin-evoked cold and mechanical allodynia, and the drug targets TRPA1 via generation of oxidative stress. Here, we have explored whether TRPA1 activation contributes to paclitaxel-induced mechanical and cold hypersensitivity and whether this activation is mediated by oxidative stress generation. Paclitaxel-evoked mechanical allodynia was reduced partially by the TRPA1 antagonist, HC-030031, and the TRPV4 antagonist, HC-067047, and was completely abated by the combination of the two antagonists. The reduced paclitaxel-evoked mechanical allodynia, observed in TRPA1-deficient mice, was completely abolished when mice were treated with HC-067047. Cold allodynia was abated completely by HC-030031 and in TRPA1-deficient mice. Exposure to paclitaxel of slices of mouse esophagus released the sensory neuropeptide, calcitonin gene-related peptide (CGRP). This effect was abolished by capsaicin desensitization and in calcium-free medium (indicating neurosecretion from sensory nerve terminals), partially reduced by either HC-030031 or HC-067047, and completely abated in the presence of glutathione (GSH). Finally, the reduced CGRP release, observed in esophageal slices of TRPA1-deficient mice, was further inhibited by GSH. Paclitaxel via oxygen radical formation targets TRPA1 and TRPV4, and both channels are key for the delayed development of mechanical allodynia. Cold allodynia is, however, entirely dependent on TRPA1.

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Section: Introductionmentioning

confidence: 78%

TRPA1 and TRPV4 mediate paclitaxel-induced peripheral neuropathy in mice via a glutathione-sensitive mechanism

Materazzi

Fusi

Benemei

et al. 2012

Pflugers Arch - Eur J Physiol

197

188

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“…The protective effect of NAC against paclitaxel-induced reduction in cell viability might be concentration-dependent, although such experiments were not carried out. It has been reported, however, that co-treatment of cancer cells (MDA-MB-435s, MDA-MB-231, and SKBR-3 cells) with the antioxidants resveratrol or vitamin E markedly abrogated the paclitaxel-induced reduction in cell viability in a concentration-dependent manner [27]. …”

Section: Discussionmentioning

confidence: 99%

N-Acetylcysteine Modulates the Cytotoxic Effects of Paclitaxel

2011

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Background: Paclitaxel is a microtubule-stabilizing drug known to cause mitotic G2/M arrest and apoptosis. It also increases the generation of reactive oxygen species (ROS) known to be involved in both apoptotic and necrotic cell death. Antioxidants, such as N-acetylcysteine (NAC), prevent the deleterious effects of ROS and modulate the regulation of apoptotic-linked cellular proteins. Methods: A549 human adenocarcinoma alveolar epithelial cells were treated with 5.0 mM NAC, 1.0 µM paclitaxel, or co-incubated with both NAC and paclitaxel for a 24-hour incubation period. The effects of NAC in paclitaxel-induced cytotoxicity were evaluated by measuring cell viability, production of ROS, and apoptosis. Results: Challenge of cells with paclitaxel resulted in time/concentration-dependent decreases in cell viability and increases in intracellular levels of ROS, and apoptosis, all effects being abrogated by co-treatment with NAC. NAC reduced the paclitaxel-induced increase in activated caspase-10 levels, but potentiated that for caspase-3. Conclusions: NAC alters the cytotoxicity of paclitaxel in vitro by decreasing the levels of ROS, preventing apoptosis, and modulating apoptotic cellular proteins.

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“…To evaluate the effect of the co-administration of guarana and antitumor agents on cell viability and proliferation, the MTT assay was used as previously described by Fukui et al (26), who investigated the effect of resveratrol and paclitaxel co-administration on the viability of several cancer cell lines with slight modifications. A total of 10 µl of MTT (at 5 mg/ml) was added to each well at a final concentration of 500 µg/ml.…”

Section: Methodsmentioning

confidence: 99%

Effect of Paullinia cupana on MCF-7 breast cancer cell response to chemotherapeutic drugs

Hertz

Cadoná

Machado

et al. 2014

Molecular and Clinical Oncology

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Abstract. Previous studies suggested that certain plants, such as guarana (Paullinia cupana), exert a protective effect against cancer-related fatigue in breast cancer patients undergoing chemotherapy. However, guarana possesses bioactive molecules, such as caffeine and catechin, which may affect the pharmacological properties of antitumor drugs. Therefore, the aim of this study was to evaluate the effects of guarana on breast cancer cell response to 7 chemotherapeutic agents currently used in the treatment of breast cancer. To perform this study, MCF-7 breast cancer cells were cultured under controlled conditions and exposed to 1, 5 and 10 µg/ml guarana concentrations, with and without chemotherapeutics (gemcitabine, vinorelbine, methotrexate, 5-fluorouracil, paclitaxel, doxorubicin and cyclophosphamide). The effect of these treatments on MCF-7 cell viability and proliferation was spectrophotometrically analyzed with the MTT assay. The main results demonstrated an antiproliferative effect of guarana at concentrations of 5 and 10 µg/ml and a significant effect on chemotherapeutic drug action. In general, guarana improved the antiproliferative effect of chemotherapeutic agents, causing a decrease of >40% in cell growth after 72 h of exposure. The results suggested an interaction of guarana with the chemotherapeutic drugs, which requires confirmation by in vivo complementary studies.

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Resveratrol attenuates the anticancer efficacy of paclitaxel in human breast cancer cells in vitro and in vivo

Cited by 114 publications

References 43 publications

TRPA1 and TRPV4 mediate paclitaxel-induced peripheral neuropathy in mice via a glutathione-sensitive mechanism

TRPA1 and TRPV4 mediate paclitaxel-induced peripheral neuropathy in mice via a glutathione-sensitive mechanism

N-Acetylcysteine Modulates the Cytotoxic Effects of Paclitaxel

Effect of Paullinia cupana on MCF-7 breast cancer cell response to chemotherapeutic drugs

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