Involvement of MAPK, Bcl‐2 family, cytochrome<i> c</i>, and caspases in induction of apoptosis by 1,6‐<i>O,O</i>‐diacetylbritannilactone in human leukemia cells

Pan, Min‐Hsiung; Chiou, Yi Siou; Cheng, An Chin; Bai, Naisheng; Lo, Chih Yu; Tan, Di; Ho, Chi‐Tang

doi:10.1002/mnfr.200600148

Cited by 36 publications

(26 citation statements)

References 36 publications

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“…Cell‐cycle analysis revealed that AS induced cell‐cycle arrest at the G 2 ‐M phase, which is accompanied by an increase in sub‐G 1 fraction, indicating apoptotic cell death. Similar results were recently reported for the sesquiterpene lactone 1,6‐ O , O ‐diacetylbritannilactone in HL‐60 cells 28.…”

Section: Discussionsupporting

confidence: 90%

Naturally occurring asteriscunolide A induces apoptosis and activation of mitogen‐activated protein kinase pathway in human tumor cell lines

Negrín

Eiroa

Morales

et al. 2010

Molecular Carcinogenesis

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Sesquiterpene lactones have attracted much attention because they display a wide range of biological activities, including antitumor properties. Here, we show the effects of the naturally occurring sesquiterpene lactone asteriscunolide A (AS) on viability of human melanoma, leukemia and cells that overexpress antiapoptotic proteins, namely Bcl-2 and Bcl-x(L). All cell lines were sensitive to this compound, with IC(50) values of approximately 5 microM. The cytotoxic effects of AS were accompanied by a G(2)-M phase arrest of the cell cycle and a concentration- and time-dependent appearance of apoptosis as determined by DNA fragmentation, translocation of phosphatidylserine to the cell surface and sub-G(1) ratio. Apoptosis was associated with caspase-3 activity and poly(ADP-ribose) polymerase cleavage and was prevented by the nonspecific caspase inhibitor z-VAD-fmk, indicating that caspases are essential components in this pathway. The apoptotic effect of AS was also associated with (i) the release of cytochrome c from mitochondria which was accompanied by dissipation of the mitochondrial membrane potential (Delta Psi(m)) and (ii) the activation of the mitogen-activated protein kinases (MAPKs) pathway. AS-induced cell death was potentiated by inhibition of extracellular signal-regulated kinases (ERK) 1/2 signaling with U0126 and PD98059. Intracellular reactive oxygen species (ROS) seem to play a pivotal role in this process since high levels of ROS were produced early (1 h) and apoptosis was completely blocked by the free radical scavenger N-acetyl-L-cysteine (NAC). The present study demonstrates that AS-induced cell death is mediated by an intrinsic-dependent apoptotic event involving mitochondria and MAPKs, and through a mechanism dependent on ROS generation.

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Section: Discussionsupporting

confidence: 90%

Naturally occurring asteriscunolide A induces apoptosis and activation of mitogen‐activated protein kinase pathway in human tumor cell lines

Negrín

Eiroa

Morales

et al. 2010

Molecular Carcinogenesis

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“…Previous studies have shown that ABL exhibit potent anti-inflammatory effects in vascular smooth muscle cells 21, 22, 23 and anticancer activities against colon, breast, ovary, leukemia and prostate cancer cells. 24, 25, 26, 27 Moreover, additional researches reported that ABL could activate caspases via the mitochondrial apoptosis pathway, induce Bcl-2 phosphorylation and suppress NF- κ B activation in several types of cell lines. 21, 25, 27 Therefore, it is interesting to investigate whether ABL could be a synergist to help increase the efficacy of other chemopreventive agents in cancer therapy.…”

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confidence: 99%

“…24, 25, 26, 27 Moreover, additional researches reported that ABL could activate caspases via the mitochondrial apoptosis pathway, induce Bcl-2 phosphorylation and suppress NF- κ B activation in several types of cell lines. 21, 25, 27 Therefore, it is interesting to investigate whether ABL could be a synergist to help increase the efficacy of other chemopreventive agents in cancer therapy. With the goal of enhancing the chemopreventive effects of celecoxib and reduced the dose in chemotherapy, we evaluated the possibility of the combination treatment of celecoxib and ABL on human breast cancer in vivo and in vitro .…”

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confidence: 99%

Celecoxib and acetylbritannilactone interact synergistically to suppress breast cancer cell growth via COX-2-dependent and -independent mechanisms

Liu

Wen

et al. 2011

Cell Death Dis

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The use of celecoxib is associated with a significant decrease in breast cancer risk. However, the long-term use of high-dose celecoxib might be limited owing to cardiovascular side effects. In this study, we found that acetylbritannilactone (ABL), extract from a Chinese medicinal herb, could reduce celecoxib dose and potentiate the growth-inhibitory effect in breast cancer cells. ABL enhanced the apoptotic effect of celecoxib in COX-2-expressing cells, but had little effect in COX-2-negative cells. The apoptosis induced by the combination treatment disappeared when COX-2 was knocked down, whereas the lack of apoptotic effects in COX-2-negative cells was reversed after COX-2 transfection. However, the combination treatment induced a G0/G1 phase arrest independent of whether or not the cells expressed COX-2. The G0/G1 arrest was attributed to a decreased expression of cyclinD1, cyclinE, CDK2 and CDK6, especially the upregulation of p21. In addition, inhibition of Akt and p38 signaling pathways was required by the synergism, as the constitutively active Akt and p38 protected cells against apoptosis and cell cycle arrest induced by the combination treatment. In vivo, administration of celecoxib and ABL were more effective than the individual agents against xenograft tumor growth. Thus, our data suggested that the combinatorial approach of celecoxib and ABL might be helpful for breast cancer treatment.

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“…In particular, relative stereochemistry was able to be assigned by Cheng et al (2012) through NOESY experiments. The NMR data are given in Table II from Inula britannica L. demonstrated strong cytotoxic activity and induction of apoptosis in HL-60 cells through the activation of caspase-8, -9, and -3, phosphorylation of Bcl-2 and Bid, and by augmenting the release of cytochrome c from mitochondria (Pan et al 2007). Acetylbritannilactone, also from Inula britannica, has enforced apoptosis in VSMC cells as shown by induction of a greater ratio of Bax/Bcl-2, activation of caspase-9, caspase-3, and the breakdown of Poly (ADP-ribose) polymerase .…”

Section: Resultsmentioning

confidence: 99%

Cytotoxic sesquiterpene lactones from the aerial parts of Inula aucheriana.

Gohari

Mosaddegh

Naghibi

et al. 2015

An. Acad. Bras. Ciênc.

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Inula aucheriana DC is a member of the family Asteraceae which is known to produce cytotoxic secondary metabolites noted as sesquiterpene lactones. In the present study, sesquiterpene lactones inuchinenolide B, 6-deoxychamissonolide (stevin) and 14-acetoxy-1β,5α,7αH-4β-hydroxy-guai-9(10),11(13)-dien-12,8α-olide were isolated from I. aucheriana. Inuchinenolide B and 14-acetoxy-1β,5α,7αH-4β-hydroxy-guai-9(10),11(13)-dien-12,8α-olide were further evaluated by the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay to demonstrate cytotoxic activity with IC 50 values of (56.6, 19.0), (39.0, 11.8), and (55.7, 15.3) μg/mL against HepG-2, MCF-7 and A-549 cells, respectively. The cytotoxic activity of the two evaluated sesquiterpene lactones partly explains the cytotoxic activity that was previously observed for the extracts of Inula aucheriana. The isolated compounds could be further investigated in cancer research studies.

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Involvement of MAPK, Bcl‐2 family, cytochrome c, and caspases in induction of apoptosis by 1,6‐O,O‐diacetylbritannilactone in human leukemia cells

Cited by 36 publications

References 36 publications

Naturally occurring asteriscunolide A induces apoptosis and activation of mitogen‐activated protein kinase pathway in human tumor cell lines

Naturally occurring asteriscunolide A induces apoptosis and activation of mitogen‐activated protein kinase pathway in human tumor cell lines

Celecoxib and acetylbritannilactone interact synergistically to suppress breast cancer cell growth via COX-2-dependent and -independent mechanisms

Cytotoxic sesquiterpene lactones from the aerial parts of Inula aucheriana.

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