Inhibitory Effect of 12-
 O
 -Tetradecanoylphorbol-13-acetate Alone or in Combination with All-
 trans
 -Retinoic Acid on the Growth of LNCaP Prostate Tumors in Immunodeficient Mice

Zheng, Xi; Chang, Richard L.; Cui, Xiaojie; Avila, Gina E.; Lee, Sabrina; Lü, Yao; Lou, You-Rong; Shih, Weichung Joe; Lin, Yong; Reuhl, Kenneth R.; Newmark, Harold L.; Rabson, Arnold B.; Conney, Allan H.

doi:10.1158/0008-5472.can-03-2848

Cited by 36 publications

(50 citation statements)

References 42 publications

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“…Mice (n ϭ 6 per group) were injected i.p. with TPA dissolved in corn oil (200 ng/g body weight, 2-h intervals), or vehicle, at 0.5 h before, and up to 4.5 h post-8.3Gy SH irradiation (38). Mice showed no signs of acute toxicity.…”

Section: Methodsmentioning

confidence: 99%

Oncogenic bystander radiation effects in Patched heterozygous mouse cerebellum

Mancuso¹,

Pasquali

Leonardi³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

240

171

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The central dogma of radiation biology, that biological effects of ionizing radiation are a direct consequence of DNA damage occurring in irradiated cells, has been challenged by observations that genetic/ epigenetic changes occur in unexposed ''bystander cells'' neighboring directly-hit cells, due to cell-to-cell communication or soluble factors released by irradiated cells. To date, the vast majority of these effects are described in cell-culture systems, while in vivo validation and assessment of biological consequences within an organism remain uncertain. Here, we describe the neonatal mouse cerebellum as an accurate in vivo model to detect, quantify, and mechanistically dissect radiation-bystander responses. DNA double-strand breaks and apoptotic cell death were induced in bystander cerebellum in vivo. Accompanying these genetic events, we report bystander-related tumor induction in cerebellum of radiosensitive Patched-1 (Ptch1) heterozygous mice after x-ray exposure of the remainder of the body. We further show that genetic damage is a critical component of in vivo oncogenic bystander responses, and provide evidence supporting the role of gap-junctional intercellular communication (GJIC) in transmission of bystander signals in the central nervous system (CNS).These results represent the first proof-of-principle that bystander effects are factual in vivo events with carcinogenic potential, and implicate the need for re-evaluation of approaches currently used to estimate radiation-associated health risks.cancer risk ͉ DNA damage ͉ in vivo ͉ medulloblastoma ͉ radiation

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Section: Methodsmentioning

confidence: 99%

Oncogenic bystander radiation effects in Patched heterozygous mouse cerebellum

Mancuso¹,

Pasquali

Leonardi³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

240

171

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show abstract

“…Apoptotic cells were determined by morphological assessment in cells stained with propidium iodide (32,33). Cytospin slides were prepared following each experiment and cells were fixed with acetone/methanol (1:1) at room temperature for 10 min, followed by 10 min of propidium iodide staining (1 µg/ml in PBS), and were then analyzed using a fluorescence microscope (Nikon Eclipse TE200, Japan).…”

Section: Assessment Of Apoptotic Cells By Morphology and Activation Omentioning

confidence: 99%

“…Cytospin slides were prepared following each experiment and cells were fixed with acetone/methanol (1:1) at room temperature for 10 min, followed by 10 min of propidium iodide staining (1 µg/ml in PBS), and were then analyzed using a fluorescence microscope (Nikon Eclipse TE200, Japan). Apoptotic cells were identified by classical morphological features, including nuclear condensation, cell shrinkage and formation of apoptotic bodies (32,33).…”

Section: Assessment Of Apoptotic Cells By Morphology and Activation Omentioning

confidence: 99%

Effects of cyclohexanone analogues of curcumin on growth, apoptosis and NF-κB activity in PC-3 human prostate cancer cells

Wei

Cui

et al. 2012

Oncology Letters

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Abstract. Curcumin is a non-nutritive yellow pigment found in the spice turmeric, which is derived from the rhizome of the plant Curcuma longa Linn. Six cyclohexanone analogues of curcumin (A 1 -A 6 ) were investigated for their effects on growth and apoptosis in PC-3 human prostate cancer cells. The ability of these compounds to inhibit NF-κB activity in PC-3 cells was also determined. Five out of the six curcumin analogues (A 2 -A 6 ) had stronger inhibitory effects compared to curcumin on the growth of cultured PC-3 cells. Compounds A 2 -A 6 also had stronger stimulatory effects on apoptosis in PC-3 cells than curcumin, and these curcumin analogues more potently inhibited NF-κB activity than curcumin. The inhibitory effects of these compounds on NF-κB activity correlated with their effects on growth inhibition and apoptosis stimulation in PC-3 cells. The results of the present study provide a rationale for in vivo studies with A 2 -A 6 using suitable animal models of prostate cancer. IntroductionCurcumin is a non-nutritive yellow pigment found in the spice turmeric, which is derived from the rhizome of the plant Curcuma longa Linn. Curcumin lacks toxicity in humans (1), and extensive research over several decades has revealed that curcumin possesses anticancer, anti-inflammatory, antioxidant, antiviral and anti-bacterial activities (2,3). Curcumin suppressed cell proliferation or induced apoptosis in cultured prostate cancer cells and other types of cancer cells (4-10). Curcumin also inhibited prostate carcinogenesis (11). Studies from our laboratory and those of other authors have demonstrated enhanced anticancer activities of curcumin when combined with other anticancer agents (12-14). Findings of earlier studies showed that curcumin exerts a wide range of anticancer effects by modulating a diversity of signaling pathways, including nuclear factor-κB (NF-κB) and other pathways (15)(16)(17)(18)(19)(20). Curcumin has entered clinical trials for certain types of human cancer (21-23). However, the clinical efficacy of curcumin is limited, which is likely to be due to its low bioavailability (21-23). It was suggested that the β-diketone moiety of curcumin causes instability and poor metabolic properties (24-26). Enhanced stability was found in curcumin analogues by deleting the β-diketone moiety of the molecule (27). Recently, it was demonstrated that the cyclohexanone analogues of curcumin have enhanced stability in biological medium compared to curcumin (28). The cyclohexanone-containing curcumin analogue 2,6-bisp[(3-methoxy-4-hydroxyphenyl)methylene)]-cyclohexanone was found to be more potent than curcumin for inhibiting NF-κB in human breast cancer cells in vitro (29).In an earlier study, we synthesized a series of cyclohexanone curcumin analogues and determined their inhibitory effect on the activity of aldose reductase (30). In the present study, we investigated the effects of these curcumin analogues on the growth and apoptosis of human prostate cancer PC-3 cells. We also determined the inhibitory effect ...

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“…[22][23][24] Combinations of TPA with other experimental therapeutics are under preclinical investigations. 25 Similarly, anticancer drugs, especially topoisomerase inhibitors, cause secondary cancers. [26][27][28][29] To complicate matters further, chemopreventive agents may promote cancer in some conditions.…”

Section: Introductionmentioning

confidence: 99%

Carcinogenesis, cancer therapy and chemoprevention

Blagosklonny

2005

Cell Death Differ

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Carcinogenesis and cancer therapy are two sides of the same coin, such that the same cytotoxic agent can cause cancer and be used to treat cancer. This review links carcinogenesis, chemoprevention and cancer therapy in one process driven by cytotoxic agents (carcinoagents) that select either for or against cells with oncogenic alterations. By unifying therapy and cancer promotion and by distinguishing nononcogenic and oncogenic mechanisms of resistance, I discuss anticancer-and chemopreventive agent-induced carcinogenesis and tumor progression and, vice versa, carcinogens as anticancer drugs, anticancer drugs as chemopreventive agents and exploiting oncogene-addiction and drug resistance for chemoprevention and cancer therapy.

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Inhibitory Effect of 12- O -Tetradecanoylphorbol-13-acetate Alone or in Combination with All- trans -Retinoic Acid on the Growth of LNCaP Prostate Tumors in Immunodeficient Mice

Cited by 36 publications

References 42 publications

Oncogenic bystander radiation effects in Patched heterozygous mouse cerebellum

Oncogenic bystander radiation effects in Patched heterozygous mouse cerebellum

Effects of cyclohexanone analogues of curcumin on growth, apoptosis and NF-κB activity in PC-3 human prostate cancer cells

Carcinogenesis, cancer therapy and chemoprevention

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