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      The natural compound Guttiferone F sensitizes prostate cancer to starvation induced apoptosis via calcium and JNK elevation

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          Abstract

          Background

          In a cytotoxicity screen in serum-free medium, Guttiferone F showed strong growth inhibitory effect against prostate cancer cells.

          Methods

          Prostate cancer cells LNCaP and PC3 were treated with Guttiferone F in serum depleted medium. Sub-G1 phase distributions were estimated with flow cytometry. Mitochondrial disruption was observed under confocal microscope using Mitotracker Red staining. Gene and protein expression changes were detected by real-time PCR and Western blotting. Ca 2+ elevation was examined by Fluo-4 staining under fluorescence microscope. PC3 xenografts in mice were examined by immunohistochemical analysis.

          Results

          Guttiferone F had strong growth inhibitory effect against prostate cancer cell lines under serum starvation. It induced a significant increase in sub-G1 fraction and DNA fragmentation. In serum-free medium, Guttiferone F triggered mitochondria dependent apoptosis by regulating Bcl-2 family proteins. In addition, Guttiferone F attenuated the androgen receptor expression and phosphorylation of ERK1/2, while activating the phosphorylation of JNK and Ca 2+ flux. Combination of caloric restriction with Guttiferone F in vivo could increase the antitumor effect without causing toxicity.

          Conclusions

          Guttiferone F induced prostate cancer cell apoptosis under serum starvation via Ca 2+ elevation and JNK activation. Combined with caloric restriction, Guttiferone F exerted significant growth inhibition of PC3 cells xenograft in vivo. Guttiferone F is therefore a potential anti-cancer compound.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s12885-015-1292-z) contains supplementary material, which is available to authorized users.

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          Most cited references39

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          Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer: updated survival in the TAX 327 study.

          Dominik R. Berthold, Gregory R. Pond, Freidele Soban … (2008)
          The TAX 327 study compared docetaxel administered every 3 weeks (D3), weekly docetaxel (D1), and mitoxantrone (M), each with prednisone (P), in 1,006 men with metastatic hormone-resistant prostate cancer (HRPC). The original analysis, undertaken in August 2003 when 557 deaths had occurred, showed significantly better survival and response rates for pain, prostate-specific antigen (PSA), and quality of life for D3P when compared with MP. Here, we report an updated analysis of survival. Investigators were asked to provide the date of death or last follow-up for all participants who were alive in August 2003. By March 2007, data on 310 additional deaths were obtained (total = 867 deaths). The survival benefit of D3P compared with MP has persisted with extended follow-up (P = .004). Median survival time was 19.2 months (95% CI, 17.5 to 21.3 months) in the D3P arm, 17.8 months (95% CI, 16.2 to 19.2 months) in the D1P arm, and 16.3 months (95% CI, 14.3 to 17.9 months) in the MP arm. More patients survived >/= 3 years in the D3P and D1P arms (18.6% and 16.6%, respectively) compared with the MP arm (13.5%). Similar trends in survival between treatment arms were seen for men greater than and less than 65 years of age, for those with and without pain at baseline, and for those with baseline PSA greater than and less than the median value of 115 ng/mL. The present analysis confirms that survival of men with metastatic HRPC is significantly longer after treatment with D3P than with MP. Consistent results are observed across subgroups of patients.
          Article 0 comments Cited 250 times – based on 0 reviews     Review now
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            Tumours with PI3K activation are resistant to dietary restriction

            Nada Kalaany, David Sabatini (2009)
            Dietary restriction (DR) delays the incidence and decreases the growth of various types of tumours, but the mechanisms underlying the sensitivity of tumours to food restriction remain unknown. We find that certain human cancer cell lines, when grown as tumour xenografts in mice, are highly sensitive to the anti-growth effects of DR, while others are resistant. Cancer cells that form DR-resistant tumours carry mutations that cause constitutive activation of the PI3K pathway and in culture proliferate in the absence of insulin or IGF1. Substitution of an activated mutant allele of PI3K with wild-type PI3K in otherwise isogenic cancer cells, or the restoration of PTEN expression in a PTEN-null cancer cell line, is sufficient to convert a DR-resistant tumour into one that is DR-sensitive. DR does not affect a PTEN-null mouse model of prostate cancer, but significantly decreases tumour burden in a mouse model of lung cancer lacking constitutive PI3K signaling. Thus, the PI3K pathway is a major determinant of the sensitivity of tumours to DR and activating mutations in the pathway may influence the response of cancers to DR-mimetic therapies.
            Article 0 comments Cited 144 times – based on 0 reviews     Review now
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              Identification of arctigenin as an antitumor agent having the ability to eliminate the tolerance of cancer cells to nutrient starvation.

              Suresh Awale, Yasuhiro Tezuka, Jie Lu … (2006)
              Tumor cells generally proliferate rapidly and the demand for essential nutrients as well as oxygen always exceeds the supply due to the unregulated growth and the insufficient and inappropriate vascular supply. However, cancer cells show an inherent ability to tolerate extreme conditions, such as that characterized by low nutrient and oxygen supply, by modulating their energy metabolism. Thus, targeting nutrient-deprived cancer cells may be a novel strategy in anticancer drug development. Based on that, we established a novel screening method to discover anticancer agents that preferentially inhibit cancer cell viability under the nutrient-deprived condition. After screening 500 medicinal plant extracts used in Japanese Kampo medicine, we found that a CH(2)Cl(2)-soluble extract of Arctium lappa exhibited 100% preferential cytotoxicity under the nutrient-deprived condition at a concentration of 50 microg/mL with virtually no cytotoxicity under nutrient-rich condition. Further bioassay-guided fractionation and isolation led to the isolation of arctigenin as the primary compound responsible for such preferential cytotoxicity; the compound exhibited 100% preferential cytotoxicity against nutrient-deprived cells at a concentration of 0.01 microg/mL. Furthermore, arctigenin was also found to strongly suppress the PANC-1 tumor growth in nude mice, as well as the growth of several of the tested pancreatic cancer cell lines, suggesting the feasibility of this novel antiausterity approach in cancer therapy. Further investigation of the mechanism of action of arctigenin revealed that the compound blocked the activation of Akt induced by glucose starvation, which is a key process in the tolerance exhibited by cancer cells to glucose starvation.
              Article 0 comments Cited 53 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Xin Li: lixin458468@126.com
                Yuanzhi Lao: Laurence_ylao@163.com
                Hong Zhang: zhnjau19851010@163.com
                Xiaoyu Wang: wangdxiaoyu@hotmail.com
                Hongsheng Tan: ths97029@163.com
                Zhixiu Lin: linzx@cuhk.edu.hk
                Hongxi Xu: xuhongxi88@gmail.com
                Journal
                Journal ID (nlm-ta): BMC Cancer
                Journal ID (iso-abbrev): BMC Cancer
                Title: BMC Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-2407
                Publication date (Electronic): 11 April 2015
                Publication date PMC-release: 11 April 2015
                Publication date Collection: 2015
                Volume: 15
                Electronic Location Identifier: 254
                Affiliations
                [ ]School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203 P.R. China
                [ ]Engineering Research Center of Shanghai Colleges for TCM New Drug Discovery, Shanghai, 201203 P.R. China
                [ ]School of Chinese Medicine, Faculty of Science, The Chinese University of Hong Kong, Shatin, N.T, Hong Kong, SAR China
                Article
                Publisher ID: 1292
                DOI: 10.1186/s12885-015-1292-z
                PMC ID: 4394563
                SO-VID: 249e194d-90a4-42f4-a628-c92a6f3f4865
                Copyright © © Li et al.; licensee BioMed Central. 2015
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 29 April 2014
                Date accepted : 30 March 2015
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2015

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: guttiferone f,prostate cancer,apoptosis,starvation,natural compound
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: guttiferone f, prostate cancer, apoptosis, starvation, natural compound

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