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2008年03月21日

【期刊论文】Saw Palmetto induces growth arrest and apoptosis of androgen-dependent prostate cancer LNCaP cells via inactivation of STAT 3 and androgen receptor signaling

杨洋, YANG YANG, TAKAYUKI IKEZOE, ZHIXING ZHENG, HIROKUNI TAGUCHI, H. PHILLIP KOEFFLER and WEI-GUO ZHU

INTERNATIONAL JOURNAL OF ONCOLOGY 31: 593-600, 2007,-0001,():

-1年11月30日

摘要

PC-SPES is an eight-herb mixture that has an activity against prostate cancer. Recently, we purified Saw Palmetto (Serenoa repens) from PC-SPES and found that Saw Palmetto induced growth arrest of prostate cancer LNCaP, DU145, and PC3 cells with ED50s of approximately 2.0, 2.6, and 3.3 μl/ml, respectively, as measured by mitochondrialdependent conversion of the the 3-(4, 5-dimethylthiazol-2-yl)- 2, 5-diphenyltetrazolium bromide (MTT) assay. Saw Palmetto induced apoptosis of LNCaP cells in a time- and dosedependent manner as measured by TUNEL assays. Also, Saw Palmetto increased the expression of p21waf1 and p53 protein in LNCaP cells. In addition, we found that Saw Palmetto down-regulated DHT- or IL-6-induced expression of prostate specific antigen in conjunction with down-regulation of the level of androgen receptor in the nucleus as measured by Western blot analysis. Moreover, Saw Palmetto downregulated the IL-6-induced level of the phosphorylated form of STAT 3 in LNCaP cells. Furthermore, Saw Palmetto inhibited the growth of LNCaP cells present as tumor xenografts in BALB/c nude mice without adverse effect. These results indicate that Saw Palmetto might be useful for the treatment of individuals with prostate cancer.

Saw Palometto, PSA,, prostate cancer, androgen receptor, STAT 3

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2008年03月21日

【期刊论文】ZD6474 induces growth arrest and apoptosis of GIST-T1 cells, which is enhanced by concomitant use of sunitinib

杨洋, Yang Yang, , Takayuki Ikezoe, Chie Nishioka, Takahiro Taguchi, Wei-guo Zhu, H. Phillip Koeffler and Hirokuni Taguchi

Cancer Sci December 2006 vol. 97 no. 12 1407,-0001,():

-1年11月30日

摘要

ZD6474 (Zactima, AstraZeneca, Macclesfield, UK) is an orally available, small-molecule inhibitor of vascular endothelial growth factor receptor-2 and epidermal growth factor receptor tyrosine kinases, with additional activity versus rearranged during transfection (RET). This study explored the effect of ZD6474 in gastrointestinal stromal tumor-T1 (GIST-T1) cells that possess a gain of function mutation in exon 11 of the c-KIT gene. ZD6474 induced growth arrest and apoptosis of GIST-T1 cells in association with blockade of c-Kit and its downstream effectors, including Akt and extracellular signal-regulated kinase (ERK). ZD6474 treatment also blocked the mammalian target of rapamycin (mTOR), which lies downstream of Akt and ERK. Interestingly, when ZD6474 was combined with sunitinib (SU11248; Sutent, Pfizer, Kalamazoo, MI, USA), a class III and V receptor tyrosine kinase inhibitor, the ZD6474-mediated growth inhibition was potentiated in association with further down-regulation of the mTOR targets p-p70S6K and p-4E-BP-1. The combination of ZD6474 and sunitinib should be investigated further. (Cancer Sci 2006; 97: 1404–1409)

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2008年03月21日

【期刊论文】Aberrant methylation in promoter-associated CpG islands of multiple genes in acute lymphoblastic leukemia

杨洋, Yang Yang, Seisho Takeuchi, Wolf K. Hofmann, Takayuki Ikezoe, Jacques J.M. van Dongen, Tomasz Szczepa

Leukemia Research 30 (2006) 98–102,-0001,():

-1年11月30日

摘要

Methylation profile was analyzed in 10 childhood acute lymphoblastic leukemia (ALL) and nine adult ALL cases. Four genes (p15, p16, RARβ, FHIT) had methylation in both diseases, four genes (p14, Rb, MLH1, DAPK) showed no methylation in both diseases, and the two genes (APC, RIZ) demonstrated methylation only in adult ALL. Methylation of the RARβ was more frequent in adult ALL than that in childhood ALL (p = 0.01). The number of patients with methylation of multiple genes was higher in adult ALL than that in childhood ALL (p = 0.006). Moreover, overall frequency of methylation was higher in adult ALL than that in childhood ALL (p = 0.01).

Methylation, Multiple genes, ALL

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2008年03月21日

【期刊论文】Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-KB signal pathways

杨洋, Takayuki Ikezoe, Yang Yang, Kentaro Bandobashi, Tsuyako Saito, Shigeki Takemoto, Hisanori Machida, Kazuto Togitani, H. Phillip Koeffler, and Hirokuni Taguchi

Mol Cancer Ther 2005;4(4). April 2005,-0001,():

-1年11月30日

摘要

This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult T-cell leukemia (MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 Mg/ mL. Terminal deoxynucleotidyltransferase–mediated dUTP nick end labeling staining showed that oridonin caused apoptosis of MT-1 cells in a time-dependent manner. We explored effects of oridonin on antiapoptotic Bcl-2 family members and found that it down-regulated levels of Mcl-1 and BCL-xL, but not Bcl-2 protein, in both MT-1 and RPMI8226 cells. Further studies found that oridonin inhibited nuclear factor-KB (NF-kB) DNA-binding activity in these cells as measured by luciferase reporter gene, ELISA-based, and electrophoretic mobility shift assays. Oridonin also blocked tumor necrosis factor-α– and lipopolysaccharide-stimulated NF-KB activity in Jurkat cells as well as RAW264.7 murine macrophages. Of note, oridonin decreased survival of freshly isolated adult T-cell leukemia (three samples), acute lymphoblastic leukemia (one sample), chronic lymphocytic leukemia (one sample), non-Hodgkin’s lymphoma (three samples), and MM (four samples) cells from patients in association with inhibition of NF-kB DNA-binding activity. On the other hand, oridonin did not affect survival of normal lymphoid cells from healthy volunteers. Taken together, oridonin might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia. [Mol Cancer Ther 2005; 4(4): 578–86]

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2008年03月21日

【期刊论文】Proteasome inhibitor PS-341 induces growth arrest and apoptosis of non-small cell lung cancer cells via the JNK/c-Jun/AP-1 signaling

杨洋, Yang Yang, Takeyuki Ikezoe, , Tsuyako Saito, Makoto Kobayashi, H. Phillip Koeffler and Hirokuni Taguchi

Cancer Sci February 2004 vol. 95 no. 2 ,-0001,():

-1年11月30日

摘要

Proteasome inhibitor PS-341 induces growth arrest and apoptosis of multiple myeloma (MM) cells via inactivation of NF-κB in vitro and has afforded some objective responses in individuals with relapsed, refractory MM. However, the activity of PS-341 against non-hematological malignancies remains to be fully elucidated. In this study, we found that PS-341 induced growth arrest and apoptosis of NCI-H520 and -H460 non-small cell lung cancer (NSCLC) cells in conjunction with markedly up-regulated levels of p21waf1 and p53, and down-regulation of bcl-2 protein in these cells. Also, PS-341 caused phosphorylation of c-Jun NH2-terminal kinase (JNK) and c-Jun, and enhanced AP-1/DNA binding activities in these cells as measured by western blotting and enzyme-linked immunosorbent assay (ELISA), respectively. Interestingly, when the JNK/ c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21waf1 in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21waf1 playing the central role. Thus, PS-341 might be useful for the treatment of individuals with NSCLC. (Cancer Sci 2004; 95: 176–180)

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  • 杨洋 邀请

    北京大学,北京

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