Correction to Prenylated Flavonoids and Resveratrol Derivatives Isolated from <i>Artocarpus communis</i> with the Ability to Overcome TRAIL Resistance

Toume, Kazufumi; Habu, Tadashi; Arai, Midori A.; Koyano, Takashi; Kowithayakorn, Thaworn; Ishibashi, Masami

doi:10.1021/acs.jnatprod.5b00061

Cited by 2 publications

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“…Furthermore, p53-independent activation of apoptosis has been shown to be induced by resveratrol; however, p53 is likely to be required for resveratrol-induced apoptosis in many cancer cell lines [27,51,52]. In cases of cancer cells that are resistant to TRAIL, a combination therapy of resveratrol with TRAIL can exert potential benefits by attenuating its resistance to TRAIL and enhancing the activation of apoptosis [53][54][55].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-κB Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers

Rasheduzzaman¹,

Jeong²,

Park³

2018

Preprint

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anticancer agent that has the potential to sensitize a wide variety of cancer or transformed cells by inducing apoptosis. However, resistance to TRAIL is a growing concern, but it can be mitigated by employing different combination therapies. Resveratrol is a polyphenolic compound annex the outpouring of p53 and its pro-apoptotic modulator PUMA. Here, we showed the p53-independent activation of apoptosis by decrease the expression of phosphorylated Akt-mediated suppression of NF-κB activation that is also substantiated with the downregulation of anti-apoptotic factors Bcl-2 and Bcl-xl in Non-Small Cell lung adenocarcinoma cells (NSCLC), resulting in an attenuation of TRAIL resistance in combined treatment. Furthermore, apoptosis was induced in TRAIL-resistant lung cancer cells via a co-treatment of resveratrol and TRAIL, which was assessed by the loss of mitochondrial membrane potential, resulting in the translocation of cytochrome c from the mitochondria into the cytosol due to mitochondrial dysfunction. Moreover, autophagy flux was not affected by resveratrol-induced TRAIL-mediated apoptosis of lung cancer cells. Overall, targeting the NF-κB (p65) pathway via resveratrol attenuates TRAIL resistance and induces TRAIL-mediated apoptosis which could be the eminent therapeutic strategy to treat lung cancer.

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Section: Introductionmentioning

confidence: 99%

Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-κB Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers

Rasheduzzaman¹,

Jeong²,

Park³

2018

Preprint

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Resveratrol induces mitochondria-mediated, caspase-independent apoptosis in murine prostate cancer cells

et al. 2017

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Found in the skins of red fruits, including grapes, resveratrol (RES) is a polyphenolic compound with cancer chemopreventive activity. Because of this activity, it has gained interest for scientific investigations. RES inhibits tumor growth and progression by targeting mitochondria-dependent or -independent pathways. However, further investigations are needed to explore the underlying mechanisms.The present study is focused on examining the role of RES-induced, mitochondria-mediated, caspase-independent apoptosis of prostate cancer cells, namely transgenic adenocarcinoma of mouse prostate (TRAMP) cells. These cells were exposed to RES for various times, and cell killing, cell morphology, mitochondrial membrane potential (Δψm), expression of Bax and Bcl2 proteins, the role of caspase-3, and DNA fragmentation were analyzed.TRAMP cells exposed to RES showed decreased cell viability, altered cell morphology, and disrupted Δψm, which led to aberrant expression of Bax and Bcl2 proteins. Furthermore, since the caspase-3 inhibitor, z-VAD-fmk (benzyloxycarbonyl-valine-alanine-aspartic acid-fluoromethyl ketone), had no appreciable impact on RES-induced cell killing, the killing was evidently caspase-independent. In addition, RES treatment of TRAMP-C1, TRAMP-C2, and TRAMP-C3 cells caused an appreciable breakage of genomic DNA into low-molecular-weight fragments.These findings show that, in inhibition of proliferation of TRAMP cells, RES induces mitochondria-mediated, caspase-independent apoptosis. Therefore, RES may be utilized as a therapeutic agent to control the proliferation and growth of cancer cells.

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Correction to Prenylated Flavonoids and Resveratrol Derivatives Isolated from Artocarpus communis with the Ability to Overcome TRAIL Resistance

Cited by 2 publications

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Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-κB Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers

Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-κB Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers

Resveratrol induces mitochondria-mediated, caspase-independent apoptosis in murine prostate cancer cells

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Correction to Prenylated Flavonoids and Resveratrol Derivatives Isolated from Artocarpus communis with the Ability to Overcome TRAIL Resistance

Cited by 2 publications

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Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-&kappa;B Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers

Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-&kappa;B Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers

Resveratrol induces mitochondria-mediated, caspase-independent apoptosis in murine prostate cancer cells

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Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-κB Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers

Mitochondrial Dysfunction and Cytochrome C Translocation Induced by Resveratrol Are Dependent on NF-κB Activity and Facilitate TRAIL Sensitivity in Human Lung Cancers