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LNCaP human prostate cancer cell

Hantz, H. L., L. F. Young, and K. R. Martin. 2005. Physiologically attainable concentrations of lycopene induce mitochondrial apoptosis in LNCaP human prostate cancer cells. Exp Biol Med (Maywood) 230(3) 171-179. [Pg.431]

Hwang, E. S. and P. E. Bowen. 2004. Cell cycle arrest and induction of apoptosis by lycopene in LNCaP human prostate cancer cells. J Med Food 7(3) 284-289. [Pg.431]

Hwang, E-S and PE Bowen. 2005b. Effects of tomato paste extracts on cell proliferation, cell-cycle arrest and apoptosis in LNCaP human prostate cancer cells. Biofactors 23 75-84. [Pg.461]

J. Fukuchl, J.M. Kokontls, R.A. Hllpakka, C.P. Chuu, S. Liao, Antiproliferative effect of liver X receptor agonists on LNCaP human prostate cancer cells, Cancer Res. 64 (2004) 7686-7689. [Pg.263]

Rybalchenko V, Prevarskaya N, Van Coppenolle F, Legrand G, Lemonnier L, Le Bour-hisX, SkrymaR (2001) Verapamil inhibits proliferation of LNCaP human prostate cancer cells influencing K+ channel gating. Mol Pharmacol 59 1376-1387... [Pg.87]

D2. Dahiya, R., Park, H. D., Cusick, J., Vessella, R. L., Fournier, G., and Narayan, P., Inhibition of tumorigenic potential and prostate-specific antigen in LNCaP human prostate cancer cell line by 13-cA-retinoic acid. Int. J. Cancer 59, 126-132 (1994). [Pg.143]

Sulforaphane has been shown to induce both apoptosis and cell cycle arrest in several cell lines, including HT29 human colon cancer cells [56], LNCaP human prostate cancer cells [57], and Jurkat human T-leukemia cells [58]. Incubation of such cells with 3-30 pM SF for 24-48 hours resulted in a dose-dependent induction of apoptosis and cell cycle arrest, showing that this compound can induce apoptosis and arrest cell growth and suggesting that this activity is unlikely to be cell type specific. There is also evidence that the concentration of SF required to induce apoptosis and cell cycle arrest may be much... [Pg.120]

PAMAM dendrimer to target prostate-specific antigen (PSA) in prostate cancer. The antibody-conjugated dendrimer has been found to bind specifically to PSA positive cells (LNCaP human prostate cancer cell lines) but not with PSA negative cells (PC-3 human prostate cancer cell lines from bone) [50],... [Pg.250]

Wang TT, Hudson TS, Wang TC, Remsberg CM, Davies NM, Takahashi Y, Kim YS, Seifried H, Vinyard BT, Perkins SN, Hursting SD (2008) Differential effects of resveratrol on androgen-responsive LNCaP human prostate cancer cells in vitro and in vivo. Carcinogenesis 29 2001-2010... [Pg.2239]

Von Holtz RL, Fink CS, Awad AB (1998) P-Sitosterol activates the sphingomyelin cycle and induces apoptosis in LNCaP human prostate cancer cells. Nutr Cancer 32(1) 8-12... [Pg.3460]

Jarry H, Thelen P, Christoffel V, Spengler B, Wuttke W. Cimicifuga racemosa extract BNO 1055 inhibits proliferation of the human prostate cancer cell line LNCaP. Phytomedicine 2005 12 178-182. [Pg.165]

CaSR may also influence the proliferative and apoptotic status of the cells indirectly via modulation of cell volume homeostasis. Indeed, stimulation of CaSR in human epithelial cells induces upregulation of volume-regulated anion channels (VRAC) via a G protein-mediated increase in intracellular cAMP (Shimizu, et al., 2000). Proliferation and apoptosis are associated with essential volume perturbations [e.g., (Lang, et al., 2000)] and VRAC, a key component of homeostatic volume regulation, has been directly implicated in proliferation (Chen, et al., 2002, Doroshenko, et al., 2001, Shen, et al., 2000, Wang, et al., 2002) and apoptosis (Lemonnier, et al., 2004, Okada, et al., 2001, Okada, et al., 2006, Shen, et al., 2002). Consequently, extracellular Ca2+ may affect carcinogenesis via the CaSR-VRAC-cell volume links. The Ca2+ -permeable store-operated channel (SOC) is directly and functionally coupled to VRAC in an androgen-dependent LNCaP human prostate cancer epithelial cell line (Lemonnier, et al., 2002), evidence for another, CaSR-unrelated, potential mechanism for extracellular Ca2+ involvement in proliferative and apoptotic events. [Pg.407]

Vanden Abeele, F., Lemonnier, L., Thebault, S., Lepage, G., Parys, J. B., Shuba, Y., Skryma, R. and Prevarskaya, N., 2004, Two types of store-operated Ca2+ channels with different activation modes and molecular origin in LNCaP human prostate cancer epithelial cells. J Biol Chem 279,... [Pg.426]

Treatment of endometrial cancer (EC) cells with clotrimazole and TRAM-34, two agents known to inhibit SK4 channels, suppressed the proliferation of EC cells and arrest the EC cell cycle at the G0/G1 phase. Similarly, downregulation of SK4 by siRNA inhibited EC cell proliferation and arrested its cell cycle at the G0/G1 phase (Wang et al. 2007). Moreover, clotrimazole also inhibits proliferation of human prostate cancer cell lines, such as LNCaP and PC-3 cells (Parihar et al. 2003). [Pg.62]

K6. Kimura, G., Kasuya, J., Giannini, S., Honda, Y., Mohan, S., et al., Insulin-like growth factor (IGF) system components in human prostatic cancer cell-lines LNCaP, DU-145, and PC-3 cells. Int. J. Urol. 3, 39-46 (1996). [Pg.149]

R2. Ravenna, L., Lubrano, C., Di Silverio, F., Vacca, A., Felli, M. P., etal., Androgenic and antian-drogenic control on epidermal growth factor, epidermal growth factor receptor, and androgen receptor expression in human prostate cancer cell line LNCaP. Prostate 26, 290—298 (1995). R3. Rechler, M. M., and Nissley, S. P., Insulin-like growth factor (IGF)/somatomedin receptor subtypes structure, function and relationships to insulin receptors and IGF carrier proteins. Horm. Res. 24, 152-159 (1986). [Pg.155]

Z5. Zhuang, S. H., and Burnstein, K. L., Antiproliferative effect of la,25-dihidroxyvitamin D3 in human prostate cancer cell line LNCaP involves reduction of cyclin-dependent kinase 2 activity and persistent G1 accumulation. Endocrinology 139, 1197-1207 (1998). [Pg.159]

GLA has been shown to inhibit 5a-reductase activity in androgen-sensitive (LNCaP) and androgen-insensitive (PC3) human-prostate cancer-cell lines (102). This observation may suggest that GLA could be acting as an anticancer agent against androgen-dependent prostate and skin cancers. [Pg.1454]

Tata DB, Dunn F, Tindall DJ (1997) Selective clinical ultrasoimd signals mediate differential gene transfer and expression in two human prostate cancer cell lines LnCap and PC-3. Biochem Biophys Res Commun 234 64-67... [Pg.485]

The major obstacle in the treatment of prostate tumor with AR antagonists is the sudden appearance of AR antagonist-resistant cells. One major molecular mechanism of such resistance is point mutation of AR, as found in the human prostate cancer cell line LNCaP. The AR of LNCaP cells possesses a point mutation T877A, and is considered to take an H12-folded conformation that... [Pg.154]

Swinnen, J. V., Esquenet, M., Goossens, K., Heyns, W. and Verhoeven, G., Androgens stimulate fatty acid synthase in the human prostate cancer cell line LNCaP, Cancer Res 57 (1997a) 1086-1090. [Pg.192]

Kampa M, Papakonstanti EA, Hatzoglou A, et al. The human prostate cancer cell line LNCaP bears functional membrane testosterone receptors that increase PSA secretion and modify actin cytoskeleton. FASEB J 2002 16 1429-1431. [Pg.2053]


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Cancer, human

Cancer, prostat

Human cancer cells

Human prostate cancer

Human prostate cancer cells

Prostate cancer

Prostate cancer cells

Prostatic cancer

Prostatic cancer humans

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