Enhancement of esculetin on Taxol-induced apoptosis in human hepatoma HepG2 cells

Kuo, Hsing‐Chun; Lee, Herng-Jiun; Hu, Chao-Chin; Shun, Han-I; Tseng, Tsui‐Hwa

doi:10.1016/j.taap.2005.06.020

Cited by 57 publications

(28 citation statements)

References 31 publications

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“…Some studies have implicated the members of MAPK family as regulators of mitochondrial-dependent apoptosis [47]. Recently, Kuo et al reported that esculetin inhibited the activation of ERK1/2 and increased the phosphorylation of JNK [8]. Therefore, we hypothesized that these signaling pathways may be involved in the esculetin-induced mitochondrial changes.…”

Section: Discussionmentioning

confidence: 88%

“…Esculetin has been shown to have an anti-inflammatory effect in the Croton oil ear test [1], anti-proliferative effects on vascular smooth muscle cells [2], inhibitory action on benzo[a]pyrene plus 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis [3] and N-methyl-N-nitrosourea-induced mammary carcinoma [4], and it is a scavenger of oxygen free radicals [5,6]. It has also been shown to induce apoptosis in various cell types, including adipocytes [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Esculetin induces mitochondria-mediated apoptosis in 3T3-L1 adipocytes

2006

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Adipose tissue mass is determined by the volume and the number of adipocytes and is subjected to homeostatic regulation involving cell death mechanisms. We investigated the effects of esculetin, a coumarin compound, on apoptotic signaling in 3T3-L1 adipocytes. Esculetin treatment induced an increase in expression of Bax with a concomitant decrease of Bcl-2 in a time-dependent manner. Esculetin treatment also resulted in translocation of cytochrome c from mitochondria to cytosol and cleavage of 116 kDa poly(ADP-ribose) polymerase (PARP)-1, resulting in the accumulation of an 85 kDa cleavage product in a caspase-dependent manner. Furthermore, esculetin selectively altered the phosphorylation state of members of the MAPK superfamily, causing dephosphorylation of extracellular signal-regulating kinase 1/2 (ERK1/2) and hyperphosphorylation of c-Jun-N-terminal kinase (JNK). In addition, an inhibitor of the JNK MAP kinase pathway, SP600125, reduced esculetin-induced cytochrome c release. These results indicate that esculetin mediated adipocyte apoptosis involves the mitochondrial pathway. Esculetin thus decreases adipocyte number by initiating this apoptotic process in 3T3-L1 adipocytes.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Esculetin induces mitochondria-mediated apoptosis in 3T3-L1 adipocytes

2006

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“…Paclitaxel has been reported to activate Akt (Mabuchi et al, 2002;Hokeness et al, 2005) and MAPK pathways (Liu et al, 2001;Kuo et al, 2006;Yagi et al, 2009) and thereby compromises its apoptotic potential, whereas inhibition of these pathways by curcumin increases susceptibility of cancer cells to chemotherapeutic agents (Bava et al, 2005;Aggarwal et al, 2006;Gagnon et al, 2008). Although activated JNK contributes to some apoptotic responses, the JNK-dependent apoptotic signaling pathways can be blocked by activation of NF-kB and Akt pathways (Xia et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Molecular evidences for the chemosensitizing efficacy of liposomal curcumin in paclitaxel chemotherapy in mouse models of cervical cancer

et al. 2011

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The microtubule-targeting antineoplastic agent, paclitaxel, is highly efficacious against a wide spectrum of human cancers. However, dose-limiting toxicity and development of drug resistance limit its clinical application. Development of novel strategies that overcome chemoresistance and sensitize cancer cells to paclitaxel can enhance the therapeutic effect of this drug. We have previously shown that curcumin, a natural polyphenol, enhances paclitaxelinduced cytotoxicity in vitro through downregulation of nuclear factor (NF)-jB and Akt pathways. This study was undertaken to determine whether this synergism exists in vivo and to elucidate the underlying molecular mechanisms. Mouse cervical multistage squamous cell carcinoma model using 3-methylcholanthrene (3-MC) and a xenograft model of human cervical cancer in nonobese diabetic severe combined immunodeficient (NOD-SCID) mice using HeLa cells were used to evaluate the synergism. We observed that the combined treatment of curcumin and paclitaxel induced a synergestic reduction in the tumor incidence as well as tumor volume of animals compared with the individual treatments of paclitaxel or curcumin, although curcumin alone could not induce any significant effect at the concentration used. The results suggest that a suboptimal concentration of curcumin augments the antitumor action of paclitaxel by downregulating the activation and downstream signaling of antiapoptotic factors and survival signals such as NF-jB, Akt and mitogen-activated protein kinases that have significant roles in proliferation, survival, angiogenesis and metastasis. This study revealed for the first time that 3-MC-induced tumorigenesis in mice is associated with a strong constitutive activation of NF-jB activity. Furthermore, we also observed that pre-exposure of carcinoma cells isolated from 3-MC-induced tumors to curcumin potentiates paclitaxel-induced apoptosis. Overall, the findings of this preclinical study provide a strong rationale for the validation of this combination through clinical trials. As curcumin could effectively downregulate all these survival signals induced by paclitaxel, we suggest it as a potent chemosensitizer to improve the therapeutic index of paclitaxel.

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“…It has also been reported to associate with the effect of antagonizing iron-chelating agents and increasing the virulence of Listeria monocytogenes (Coulanges et al, 1996), preventing liver damage (Gilani et al, 1998), suppressing proteoglycan metabolism (Watanabe et al, 1999) as well as protecting against linoleic acid hydroperoxide-induced cytotoxicity (Kaneko et al, 2003) and oxidative DNA damage (Tahara et al, 2005). Especially, esculetin also exhibits effect on some kinds of cancer cells, such as human leukemia cells Chu et al, 2001) and hepatoma HepG2 cells (Kuo et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Antioxidant activity and inhibition effect on the growth of human colon carcinoma (HT-29) cells of esculetin from Cortex Fraxini

Wang

Zhang²,

Ekunwe

et al. 2010

Med Chem Res

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Esculetin was isolated from Cortex fraxini and identified by UV, IR, 1 H NMR, 13 C NMR. Its antioxidant properties were investigated employing various in vitro assays, such as 2,2 0 -diphenyl-1-picrylhydrazyl (DPPH) radical scavenging assay, hydroxyl radical scavenging assay in a new resonance scattering (RS) method, reducing power and total antioxidant assay. Esculetin showed excellent antioxidant properties superior to synthetic antioxidant butylated hydroxytoluene (BHT). Subsequently, inhibition effect of esculetin on human colon carcinoma (HT-29) cells proliferation was measured by thymidine incorporation assay. HT-29 cell number was decreasing with increasing concentration of esculetin at the lower concentrations of 0.25, 0.5, 1.0, and 2.0 mg/ml, compared to the positive control and HT-29 cells were stimulated in response to treatment with esculetin which decreases in a dose-dependent manner. However, at the higher concentrations of 4.0, 8.0, 12.0 and 16.0 mg/ml, growth of HT-29 cells were inhibited in a concentration-dependent fashion.

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Enhancement of esculetin on Taxol-induced apoptosis in human hepatoma HepG2 cells

Cited by 57 publications

References 31 publications

Esculetin induces mitochondria-mediated apoptosis in 3T3-L1 adipocytes

Esculetin induces mitochondria-mediated apoptosis in 3T3-L1 adipocytes

Molecular evidences for the chemosensitizing efficacy of liposomal curcumin in paclitaxel chemotherapy in mouse models of cervical cancer

Antioxidant activity and inhibition effect on the growth of human colon carcinoma (HT-29) cells of esculetin from Cortex Fraxini

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