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      β-Bourbonene attenuates proliferation and induces apoptosis of prostate cancer cells

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          Abstract

          Sesquiterpenes have antitumor, anti-inflammation, and anti-fungal effects. β-bourbonene is a kind of sesquiterpene, but its pharmacological effect has not been studied. The present study was conducted in order to investigate the potential anticancer effects of β-bourbonene on human prostate cancer PC-3M cells. PC-3M cells were incubated with 0, 25, 50, 100 µg/ml of β-bourbonene. Cell Counting Kit-8 (CCK-8) detection showed that compared with the control group, β-bourbonene inhibited the growth of PC-3M cells in a dose-dependent manner. G0/G1 phase arrest was observed by β-bourbonene by using flow cytometry. TUNEL staining and Annexin V/PI dual-staining method revealed that apoptosis was found in cells with β-bourbonene treatment, and the quantity of apoptotic cells was increased with the elevation in concentration. The mRNA and protein expression levels of Fas and FasL in the drug-treatment group were significantly elevated. Furthermore, the western blot assay also indicated that with an increase in the concentration of β-bourbonene, the protein expression of Bax in the drug-treatment group was significantly elevated, while a decrease was identified in the protein expression of Bcl-2. Taken together, β-bourbonene can inhibit the proliferation and simultaneously, induce apoptosis and G0/G1 arrest of prostate cancer PC-3M cells, which may be realized by upregulation of mRNA expression of Fas and FasL, increase of Bax protein expression and decrease of Bcl-2 protein expression.

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          Most cited references 24

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          Cancer statistics, 2008.

          Each year, the American Cancer Society estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute, Centers for Disease Control and Prevention, and the North American Association of Central Cancer Registries and mortality data from the National Center for Health Statistics. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,437,180 new cancer cases and 565,650 deaths from cancer are projected to occur in the United States in 2008. Notable trends in cancer incidence and mortality include stabilization of incidence rates for all cancer sites combined in men from 1995 through 2004 and in women from 1999 through 2004 and a continued decrease in the cancer death rate since 1990 in men and since 1991 in women. Overall cancer death rates in 2004 compared with 1990 in men and 1991 in women decreased by 18.4% and 10.5%, respectively, resulting in the avoidance of over a half million deaths from cancer during this time interval. This report also examines cancer incidence, mortality, and survival by site, sex, race/ethnicity, education, geographic area, and calendar year, as well as the proportionate contribution of selected sites to the overall trends. Although much progress has been made in reducing mortality rates, stabilizing incidence rates, and improving survival, cancer still accounts for more deaths than heart disease in persons under age 85 years. Further progress can be accelerated by supporting new discoveries and by applying existing cancer control knowledge across all segments of the population.
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            Environmental and heritable factors in the causation of cancer--analyses of cohorts of twins from Sweden, Denmark, and Finland.

            The contribution of hereditary factors to the causation of sporadic cancer is unclear. Studies of twins make it possible to estimate the overall contribution of inherited genes to the development of malignant diseases. We combined data on 44,788 pairs of twins listed in the Swedish, Danish, and Finnish twin registries in order to assess the risks of cancer at 28 anatomical sites for the twins of persons with cancer. Statistical modeling was used to estimate the relative importance of heritable and environmental factors in causing cancer at 11 of those sites. At least one cancer occurred in 10,803 persons among 9512 pairs of twins. An increased risk was found among the twins of affected persons for stomach, colorectal, lung, breast, and prostate cancer. Statistically significant effects of heritable factors were observed for prostate cancer (42 percent; 95 percent confidence interval, 29 to 50 percent), colorectal cancer (35 percent; 95 percent confidence interval, 10 to 48 percent), and breast cancer (27 percent; 95 percent confidence interval, 4 to 41 percent). Inherited genetic factors make a minor contribution to susceptibility to most types of neoplasms. This finding indicates that the environment has the principal role in causing sporadic cancer. The relatively large effect of heritability in cancer at a few sites suggests major gaps in our knowledge of the genetics of cancer.
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              Molecular determinants of resistance to antiandrogen therapy.

              Using microarray-based profiling of isogenic prostate cancer xenograft models, we found that a modest increase in androgen receptor mRNA was the only change consistently associated with the development of resistance to antiandrogen therapy. This increase in androgen receptor mRNA and protein was both necessary and sufficient to convert prostate cancer growth from a hormone-sensitive to a hormone-refractory stage, and was dependent on a functional ligand-binding domain. Androgen receptor antagonists showed agonistic activity in cells with increased androgen receptor levels; this antagonist-agonist conversion was associated with alterations in the recruitment of coactivators and corepressors to the promoters of androgen receptor target genes. Increased levels of androgen receptor confer resistance to antiandrogens by amplifying signal output from low levels of residual ligand, and by altering the normal response to antagonists. These findings provide insight toward the design of new antiandrogens.
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                Author and article information

                Affiliations
                Department of Urology, Sixth People's Hospital South Campus Affiliated to Shanghai Jiaotong University, Shanghai 201499, P.R. China
                Author notes
                Correspondence to: Dr Ji-Zhong Jin, Department of Urology, Sixth People's Hospital South Campus Affiliated to Shanghai Jiaotong University, 6600 Nanfeng Road, Shanghai 201499, P.R. China, E-mail: jinjizhong1016@ 123456163.com
                Journal
                Oncol Lett
                Oncol Lett
                OL
                Oncology Letters
                D.A. Spandidos
                1792-1074
                1792-1082
                October 2018
                20 July 2018
                20 July 2018
                : 16
                : 4
                : 4519-4525
                6126340 10.3892/ol.2018.9183 OL-0-0-9183
                Copyright: © Wang et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                Categories
                Articles

                Oncology & Radiotherapy

                bax/bcl-2, pc-3m, proliferation, cell cycle, apoptosis, fas/fasl, β-bourbonene

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