Improved therapeutic effectiveness by combining liposomal honokiol with cisplatin in lung cancer model

Jiang, Qiqi; Fan, Lijun; Yang, Guangli; Guo, Wenhao; Hou, Wen-Li; Chen, Lijuan; Wei, Yuquan

doi:10.1186/1471-2407-8-242

Cited by 76 publications

(72 citation statements)

References 28 publications

(38 reference statements)

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“…In addition, honokiol has a more obvious apoptosis-inducing effect on B-CLL cells than on normal mononuclear leukocytes (40). In vivo, honokiol was highly effective against SVR angiosarcoma (41) and breast cancer in nude mice (42) and in a human A549 lung cancer xenograft model (43) with the increased induction of apoptosis.…”

Section: Targeting Apoptosis Pathways In Cancer With Magnolol and Honmentioning

confidence: 91%

Targeting apoptosis pathways in cancer with magnolol and honokiol, bioactive constituents of the bark of <i>Magnolia officinalis </i>

Tang

Du³

et al. 2011

DD&T

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Magnolol and honokiol, main active compounds from the bark of Magnolia officinalis, have been found to have various pharmacological actions, including anti-oxidative, anti-inflammatory, anti-tumor, and anti-microbial properties, without appreciable toxicity. Recently, the anti-tumor activity of magnolol and honokiol has been extensively investigated. Magnolol and honokiol were found to possess anti-tumor activity by targeting the apoptosis pathways, which have been considered as targets for cancer therapies. This review will focus on the mechanisms by which magnolol and honokiol act on apoptosis pathways in cancer that have been characterized thus far, including the death receptormediated pathway, mitochondria-mediated pathway, caspase-mediated common pathway, and regulation of apoptosis-related proteins. These breakthrough findings may have important implications for targeted cancer therapy and modern applications of traditional Chinese medicine.

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Section: Targeting Apoptosis Pathways In Cancer With Magnolol and Honmentioning

confidence: 91%

Targeting apoptosis pathways in cancer with magnolol and honokiol, bioactive constituents of the bark of <i>Magnolia officinalis </i>

Tang

Du³

et al. 2011

DD&T

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“…36 In some studies, apoptosis has been demonstrated to occur weeks after cisplatin treatment. [37][38][39] In such experiments, it is not clear whether apoptosis is due to cisplatininduced signaling events or merely a passive effect [i.e., whether apoptosis is the primary cell death mechanism induced by druginduced signaling, or is a secondary effect induced by lethal cell damage (i.e. a ''funeral'' mechanism); see Ref.…”

Section: Discussionmentioning

confidence: 99%

Restriction of cisplatin induction of acute apoptosis to a subpopulation of cells in a three‐dimensional carcinoma culture model

Fayad

Brnjic

Berglind

et al. 2009

Intl Journal of Cancer

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Cisplatin is a clinically important chemotherapeutical agent used to treat epithelial malignancies. High concentrations (20-100 lM) of cisplatin have been used in numerous studies to induce apoptosis of carcinoma cells grown in monolayer culture over 24-48 hr. These conditions may not be relevant to 3-D tumor tissue in vivo and the importance of apoptosis for tumor response is controversial. We here studied the effects of cisplatin on a 3-D colon carcinoma in vitro model (multicellular spheroids). Cisplatin at a dose of 40 lM induced active caspase-3 preferentially in the peripheral 30 lm cell layer of spheroids, mainly during late stages (72-96 hr). The p53 response to cisplatin was also largely confined to peripheral cell layers. Despite the use of a high cisplatin concentration, a significant fraction of the cells in the spheroids survived treatment. A high proportion of surviving cells stained positive for b-galactosidase, a marker of premature senescence. Cells growtharrested by cisplatin treatment showed a higher spontaneous cell death rate than untreated proliferating cells. We propose that acute apoptosis is of minor significance for the overall response of carcinoma cells to cisplatin treatment. ' UICCKey words: cisplatin; apoptosis; senescence; p21Cip1; p27Kip1 Platinum derivatives are important chemotherapeutical agents for many epithelial malignancies, including testicular, ovarian, squamous cell and colon cancers.1,2 In the low intracellular chloride concentrations, cisplatin undergoes equation to form molecules that are reactive with cellular macromolecules. Cisplatin forms covalent bonds to the N7 positions of DNA purines leading to formation intra-or interstrand crosslinks, but also reacts with RNA and protein. 3,4 Treatment of tumor cells in vitro with cisplatin results in apoptosis within 24-48 hr.4-6 Dysregulation of apoptosis pathways is generally assumed to be important for resistance to cisplatin.6 Cisplatin-induced calcium signaling, leading to activation of calpain and cleavage of Bid, 7 and sustained activation of N-terminal-c-Jun kinase, 8 is important for apoptosis signaling. Recent work has shown that cisplatin is able to induce caspase activation in enucleated cells, demonstrating that cisplatin can trigger apoptosis pathways that are independent of its effects on nuclear DNA.9,10 This cytoplasmic pathway involves reactive oxygen species (ROS) and calcium signaling.10 According to one model, ROS induces activation of Bak, leading to VDAC1 and Bax activation. 11Despite the very large number of studies in this area (2,970 articles on MedLine on cisplatin/apoptosis March 2009), it is controversial whether apoptosis is the primary mode of cell death of human carcinoma cells in response to DNA damaging therapeutic drugs, and also whether apoptosis is necessary for the therapeutic effect of such drugs. 10,[12][13][14][15][16] The importance of apoptosis appears to be most pronounced in short-term experiments (1-2 days) and is of lower significance when cell viability is examined after lo...

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“…For patients with Barrett's-associated esophageal adenocarcinoma, furthermore, our finding that honokiol limits anchorage-independent growth in cancer cells suggests that this agent might be a useful cancer treatment. Other studies have shown that honokiol enhances the tumor-killing effects of a number of chemotherapeutic agents, including cisplatin, a drug used frequently in the treatment of esophageal adenocarcinoma (11,15).…”

Section: Discussionmentioning

confidence: 99%

Targeting the intrinsic inflammatory pathway: honokiol exerts proapoptotic effects through STAT3 inhibition in transformed Barrett's cells

Zhang

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Improved therapeutic effectiveness by combining liposomal honokiol with cisplatin in lung cancer model

Cited by 76 publications

References 28 publications

Targeting apoptosis pathways in cancer with magnolol and honokiol, bioactive constituents of the bark of <i>Magnolia officinalis </i>

Targeting apoptosis pathways in cancer with magnolol and honokiol, bioactive constituents of the bark of <i>Magnolia officinalis </i>

Restriction of cisplatin induction of acute apoptosis to a subpopulation of cells in a three‐dimensional carcinoma culture model

Targeting the intrinsic inflammatory pathway: honokiol exerts proapoptotic effects through STAT3 inhibition in transformed Barrett's cells

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