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Activation of Nuclear Factor-KB Contributes to Induction of Death Receptors and Apoptosis by the Synthetic Retinoid CD437 in DU145 Human Prostate Cancer Cells

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Activation of Nuclear Factor-KB Contributes to Induction of Death Receptors and Apoptosis by the Synthetic Retinoid CD437 in DU145 Human Prostate Cancer Cells Research Article Activation of Nuclear Factor-KB Contributes to Induction of Death Receptors and Apoptosis by the Synthetic Retinoid CD437 in DU145 Human Prostate Cancer Cells Fengshuo Jin,1 Xiangguo Liu,2 Zhongmei Zhou,2 Ping Yue,2 Reuben Lotan,3 Fadlo R. Khuri,2 Leland W.K. Chung,1 and Shi-Yong Sun2 Departments of 1Urology and 2Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia and 3Department of Thoracic/Head and Neck Medical Oncology, M.D. Anderson Cancer Center, Houston, Texas Abstract of multiple antiapoptotic genes, such as Bcl-2 and Bcl-XL. However, n Activation of the transcription factor, nuclear factor-KB(NF-KB), increasing evidence suggests the opposite role of NF- B activation results in up-regulation of not only antiapoptotic genes but by up-regulating the expression of some proapoptotic genes during induction of apoptosis by certain stimuli (1, 2). One example is also proapoptotic genes, including death receptor 4 (DR4) and n death receptor 5 (DR5). Therefore, NF-KB activation either that NF- B activation induces the expression of both death suppresses or promotes apoptosis depending on the type of receptor 4 (DR4) and death receptor 5 (DR5) genes, leading to stimulus or cell context. We showed previously that the enhancement of tumor necrosis factor (TNF)–related apoptosis- inducing ligand (TRAIL)–induced apoptosis (3). Many studies have synthetic retinoid, 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2- n naphthalene carboxylic acid (CD437), effectively induces shown that NF- B activation in human prostate cancer represents apoptosis particularly in androgen-independent prostate a survival pathway leading to resistance to apoptosis, whereas inhibition of NF-nB by either small molecules or dominant-negative carcinoma cells. This effect was associated with the ability of n a CD437 to induce the expression of DR4 and DR5. In the I B mutant often sensitizes prostate cancer cells to apoptosis K induced by various agents, including TNF-a, taxanes, and other present study, we examined the hypothesis that NF- B n activation plays a role in CD437-induced death receptor cytotoxic agents (4–11). However, proapoptotic effects of NF- B expression and apoptosis. Treatment of DU145 cells with activation in prostate cancer cells have also been reported (12, 13). n a CD437 resulted in a rapid decrease (z3 hours) of IKBA, which For example, LNCaP cells stably expressing I B superrepressor K (SR-InBa) exhibited resistance to apoptosis induced by TNF-a (12). was accompanied by increased translocation of the NF- B n subunit p65 from the cytoplasm to the nucleus and increased Therefore, it seems that the role of NF- B in regulation of apoptosis NF-KB DNA-binding activity (z4 hours). The NF-KB inhibitor, is agent dependent or cell context dependent. helenalin, inhibited CD437-induced IKBA reduction and p65 Retinoids, a class of natural and synthetic vitamin A analogues, nuclear translocation. Accordingly, it also abrogated CD437- have been shown to be effective in prostate cancer prevention and induced up-regulation of DR4, activation of caspase-8 and treatment in vitro, in animal models, and in clinical trials (14, 15). caspase-3, and increased DNA fragmentation. Overexpression Recently, the novel synthetic retinoid, 6-[3-(1-adamantyl)-4-hydrox- yphenyl]-2-naphthalene carboxylic acid (CD437), has attracted of an IKBA dominant-negative mutant blocked not only CD437-induced p65 nuclear translocation but also DR4 up- more attention because it is a potent inducer of apoptosis in a regulation, caspase activation, and DNA fragmentation. CD437 variety of cancer cell lines, including prostate cancer cells (15, 16) was unable to decrease IKBA protein levels and up-regulate and is effective in inhibiting tumor growth in animal models DR4 expression in CD437-resistant DU145 cells. Moreover, (17, 18). Importantly, this agent selectively induces apoptosis in knockdown of Fas-associated death domain, caspase-8, and human cancer cells while sparing their normal counterparts DR4, respectively, suppressed CD437-induced apoptosis. Col- (19, 20), warranting further evaluation of its clinical potential as lectively, these results indicate that CD437 activates NF-KB via a cancer therapeutic agent. decreasing IKBA protein and thereby induces DR4 expression CD437 preferentially induces apoptosis in androgen-indepen- and subsequent apoptosis in DU145 cells. (Cancer Res 2005; dent prostate cancer cells, although it also kills androgen- 65(14): 6354-63) dependent cancer cells (21) and is ineffective in inducing apoptosis of normal prostate epithelial cells.4 Moreover, it augments TRAIL- induced apoptosis only in androgen-independent prostate cancer Introduction cells (21). Thus, CD437 and its analogues may have potential as Nuclear factor-nB (NF-nB) activation is thought to be associated excellent candidate drugs for therapy of prostate cancer, particu- with cell resistance to apoptosis via up-regulation of the expression larly androgen-independent prostate cancer, either alone or in combination with other agents, such as TRAIL. The mechanisms by which CD437 induces apoptosis in human Note: F. Jin and X. Liu contributed equally to this work and thus share equal first cancer cells remain unclear (16, 22, 23). Like other chemothera- authorship. F. Jin is currently at the Department of Urology, Daping Hospital, peutic agents, CD437 has been reported to increase NF-nB activity Chongqing, Sichun, People’s Republic of China. F.R. Khuri, L.W.K. Chung, and S-Y. Sun in CD437-sensitive but not CD437-resistant leukemia cell lines (24). are the Georgia Cancer Coalition Distinguished Cancer Scholars. Requests for reprints: Shi-Yong Sun, Department of Hematology and Oncology, Winship Cancer Institute, Emory University School of Medicine, 1365-C Clifton Road, C3088, Atlanta, GA 30322. Phone: 404-778-2170; Fax: 404-778-5520; E-mail: [email protected]. I2005 American Association for Cancer Research. 4 S-Y. Sun et al., unpublished data. Cancer Res 2005; 65: (14). July 15, 2005 6354 www.aacrjournals.org Downloaded from cancerres.aacrjournals.org on September 27, 2021. © 2005 American Association for Cancer Research. NF-kB-Mediated Induction of Apoptosis by CD437 Moreover, other apoptosis-inducing synthetic retinoids, which are Detection of apoptosis. Cells were seeded in 96-well plates and treated structurally related to CD437, have been shown to inhibit TNF-a- with the given agents on the second day. After 24-hour treatment, cells were induced NF-nB activation in several solid cancer cell lines, which subjected to measurement of DNA fragmentation by detecting cytoplasmic may account for induction of apoptosis by these agents (25). histone-associated DNA fragments (mononucleosome and oligonucleo- somes) formed during apoptosis using a Cell Death Detection ELISAPlus kit Therefore, it is important to understand the role of NF-nB in the (Roche Molecular Biochemicals, Indianapolis, IN) according to the process of apoptosis induced by CD437. manufacturer’s instructions. In addition, we detected cleavage of caspases Our previous study has shown that CD437 effectively induces and PARP as another indicator of apoptosis using Western blot analysis as apoptosis in DU145 human prostate cancer cells, which is described below. accompanied by an up-regulation of death receptor mRNAs, Western blot analysis. The procedures for preparation of whole-cell including DR4 and DR5 (21). The current study addresses the protein lysates and for Western blotting were described previously (28). question whether CD437 induces NF-nB activation and, if so, Whole-cell protein lysates (50 Ag) were electrophoresed through 7.5% to what role of NF-nB activation plays in death receptor up- 12% denaturing polyacryamide slab gels and transferred to an Immuno-Blot regulation and apoptosis induction by CD437 using DU145 cell polyvinylidene difluoride membrane (Bio-Rad, Hercules, CA) by electro- line as a system. Our results indicate that CD437 activates NF- blotting. The blots were probed or reprobed with the primary antibodies; then, antibody binding was detected using secondary antibodies and the nB via decreasing InBa levels and this effect is actually required SuperSignal West Pico Chemiluminescent Substrate (Pierce Biotechnology, for CD437-induced DR4 up-regulation and apoptosis, thus Inc., Rockford, IL) according to the manufacturer’s protocol. highlighting a novel mechanism underlying CD437-induced Northern blot analysis. Total cellular RNA was prepared using apoptosis. TriReagent (Sigma Chemical) for Northern blot analysis as described previously (29). Total cellular RNA (30 Ag) was loaded in each lane. Human DR5 cDNA was obtained from Dr. W.S. El-Deiry (University of Pennsylvania Materials and Methods School of Medicine, Philadelphia, PA). Human DR4 cDNA was purchased Reagents. CD437 was provided by Galderma R&D (Sophia Antipolis, from Alexis Biochemicals. Glyceraldehyde-3-phosphate dehydrogenase France). The NF-nB inhibitor, helenalin (26), was purchased from Biomol cDNA probe was purchased from Ambion, Inc. (Austin, TX). (Plymouth Meeting, PA). All these agents were dissolved in DMSO at a Adenoviral infection. Adenovirus harboring an empty vector (Ad-CMV) concentration of 10 or 20 mmol/L and stored in the dark at À80jC. Stock or a dominant-negative InBa mutant (Ad-SR-InBa; ref. 30) was generously solution was diluted to the desired final concentrations with growth medium provided by M.W. Mayo (University of Virginia School of Medicine,
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