朱孝峰
肿瘤信号转导途径及靶向肿瘤异常信号转导途径的药物研究。
个性化签名
- 姓名:朱孝峰
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师, 教育部“新世纪优秀人才支持计划”入选者
- 职称:-
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学科领域:
肿瘤学
- 研究兴趣:肿瘤信号转导途径及靶向肿瘤异常信号转导途径的药物研究。
朱孝峰,研究员,博士生导师。男,1970年9月出生。中山大学肿瘤防治中心华南肿瘤学国家重点实验室课题负责人之一。中山医科大学(现中山大学)肿瘤学博士研究生毕业。2000年在美国乔治城大学癌症中心结构生物学与抗癌药物研究实验室学习。荣获第六届中国药理学会SERVIER青年药理学工作者奖。《癌症》杂志常务编务、《防癌报》编委,《中国科学》、《科学通报》、《Acta Pharmacologica Sinica》、《Planta Med》等杂志特约审稿人。近几年来先后承担国家自然科学基金四项,国家高新技术发展计划(863计划)分题,广东省自然科学基金,广东省科技计划项目,广州市科技计划项目等项目。发表论文40余篇,其中在国际SCI收录杂志发表论文19篇,主编专著二部。申请专利五项,其中二项为国际专利,二项中国发明专利已获授权。作为主要研究人员之一完成的阿诺宁脂肪乳注射液抗肿瘤作用研究已转让企业开发。主要从事研究领域包括:肿瘤信号转导途径及靶向肿瘤异常信号转导途径的药物研究。
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朱孝峰, J-M Zhou, X-F Zhu, Y-J Lu, R Deng, Z-S Huang, Y-P Mei, Y Wang, W-L Huang, Z-C Liu, L-Q Gu and Y-X Zeng
Oncogene(2006)25, 503-511,-0001,():
-1年11月30日
Agents stabilizing G-quadruplexes have the potential to interfere with telomere replication by blocking the elongation step catalysed by telomerase or telomerase-independent mechanism and could therefore act as antitumor agents. In this study, we found that quindoline derivatives interacted preferentially with intramolecular G-quadruplex structures and were novel potent telomerase inhibitors. Treatment with quindoline derivatives reproducibly inhibited telomerase activity in human leukemia K562 cells and colon cancer SW620 cells. N0-(10H-Indolo [3,2-b] quinolin-11-yl)-N, Ndimethyl-propane-1,3-diamine (SYUIQ-5), (one of quindoline derivatives), when added to K562 and SW620 cell culture at nonacute cytotoxic concentrations, increased time of population doublings of K562 and SW620 cells, induced a marked cessation in cell growth and cellular senescence phenotype after 35 and 18 days, respectively. Growth cessation was accompanied by a shortening of telomere length, and induction of p16, p21 and p27 protein expression. However, another compound SYUIQ-7 with greater IC50 for telomerase had no obvious cellular effect in nonacute cytotoxic concentrations. These results indicate that quindoline derivatives as novel potent G-quadruplex interactive agents induce senescence and telomere shortening in cancer cells and therefore are promising agents for cancer treatment. Oncogene (2006) 25, 503-511. doi:10.1038/sj.onc.1209067; published online 19 September 2005
G-quadruplex, telomerase inhibition, senescence
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朱孝峰
,-0001,():
-1年11月30日
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朱孝峰, Yu-Ping Mei, Xiao-Feng Zhu*, Jun-Min Zhou, He Huang, Rong Deng, Yi-Xin Zeng
Cancer Letters 232(2006)189-198,-0001,():
-1年11月30日
Epstein-Barr Virus (EBV) is closely associated with B cell malignancies. However, whether EBV appears to be absolutely required for cell proliferation and survival in lymphoma cells is still unknown. In this study, small interfering RNA (siRNA) targeting LMP1 was employed to investigate the effect of LMP1 on cell proliferation in EBV-positive lymphoblastoid B-cell line. A plasmid stable encoding 21-nt small RNA specifically and efficiently interfering LMP1 was constructed, resulting in a substantial loss of LMP1 mRNA and a significantly decreased LMP1 protein expression. Our data demonstrated that cell proliferation was completely inhibited and apoptosis was induced after knockdown of LMP1 gene in lymphoblastoid B-cell line. Also, we found that suppression of LMP1 caused downregulation of telomerase protein expression and decreased telomerase activity in lymphoma cells. In EBV-negative NPC cell line, transfection of plasmid expressing LMP1 greatly enhanced telomerase protein expression. Our results suggested that siRNA targeting LMP1 can induce apoptosis in EBVpositive lymphoma cells and is associated with inhibition of telomerase activity and expression. siRNA-directed LMP1 silencing may be of the therapeutic value for preventing and treating those EBV-associated tumors.
Epstein-Barr virus LMP1, siRNA, Lymphoma, Cell proliferation, Telomerase
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朱孝峰, Jin-Jun Zhu a, Fo-Bao Li a, Xiao-Feng Zhu b, *, Wei-Ming Liao a, *
Life Sciences 78(2006)1469-1477,-0001,():
-1年11月30日
p33ING1b induces cell cycle arrest and stimulates DNA repair, apoptosis and chemosensitivity. The magnitude of some p33ING1b effects may be due to activation of the tumor suppressor p53. To investigate if the p33ING1b protein affected chemosensitivity of osteosarcoma cells, we overexpressed p33ING1b in p53+/+ U2OS cells or in p53-mutant MG63 cells, and then assessed for growth arrest and apoptosis after treatment with etoposide. p33ING1b increased etoposide-induced growth inhibition and apoptosis to a much greater degree in p53+/+ U2OS cells than in p53-mutant MG63 cells. Moreover, ectopic expression of p33ING1b markedly upregulated p53, p21WAF1 and bax protein levels and activated caspase-3 protein kinase in etoposide-treated U2OS cells. Together, our data indicate that p33ING1b prominently enhances etoposide-induced apoptosis through p53-dependent pathways in human osteosarcoma cells. p33ING1b may be an important marker and/or therapeutic target in the prevention and treatment of metastatic osteosarcoma.
p33ING1b, Etoposide, p53, Apoptosis, Osteosarcoma
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【期刊论文】Ceramide induces cell cycle arrest and upregulates p27kip in nasopharyngeal carcinoma cells
朱孝峰, Xiao-Feng Zhu, Zong-Chao Liu, Bin-Fen Xie, Gong-Kan Feng, Yi-Xin Zeng*
Cancer Letters 193(2003)149-154,-0001,():
-1年11月30日
Ceramide mediates differentiation, growth arrest, apoptosis, proliferation, cytokine biosynthesis and secretion, and a variety of other cellular functions. However, little is known regarding ceramide signaling linked to the cell cycle. In the present study, the effect of ceramide on cell cycle in nasopharyngeal carcinoma cell line CNE2 was investigated. The results showed that ceramide inhibited cell proliferation and induced cell cycle arrest in G1 phase in CNE2 cells. Exposure of CNE2 cells to ceramide resulted in a dose-dependent up-regulation of the cyclin-dependent kinase inhibitor p27 and a decrease of phospho-Akt without reduced expression of total AKT protein. The activation of phosphatidylinositol-3-kinase (PI3K) and the protein expression of PTEN were unaffected following ceramide treatment. We concluded that ceramide induced cell cycle arrest in G1 phase in CNE2 cells and p27 up-regulation was involved in this process. In addition, up-regulation of p27 resulting from ceramide treatment may be due to the interruption of Akt, but decrease of phospho-Akt is independent of PI3K function or PTEN protein expression.
Nasopharyngeal carcinoma, AKT, Ceramide, Cell cycle, P27kip
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朱孝峰, Xiao-Feng Zhua, Zong-Chao Liua, Bin-Fen Xiea, Zhi-Ming Lia, Gong-Kan Fenga, Dajun Yangb, Yi-Xin Zenga, *
Cancer Letters 169(2001)27-32,-0001,():
-1年11月30日
Nasopharyngeal carcinoma (NPC), which occurs with a high incidence in southern China and southeast Asia, is of epithelial origin with overexpression of EGF receptor. To study the effect of inhibition of EGFR signaling on nasopharyngeal carcinoma cell proliferation and cell cycle distribution, EGFR tyrosine kinase inhibitor AG1478 was employed to treat Nasopharyngeal Carcinoma CNE2 cells. The results showed that AG1478 inhibited proliferation of CNE2 cells. Immunoblot showed that AG1478 inhibited EGFR phosphorylation in CNE2 cells without reduced expression of EGFR protein. The activation of Akt and MAPK which are downstream molecules of EGFR signaling pathway, were also inhibited by AG1478. AG1478 induced cell cycle arrest in G1 phase, and the levels of protein p27 were signi®cantly up-regulated. We concluded that inhibition of the EGFR signaling induced cell cycle arrest in G1 phase in CNE2 cells and p27 up-regulation was involved in this process. The EGFR kinase speci®c inhibitor is of potential to be developed into drugs for NPC treatment. q 2001 Elsevier Science Ireland Ltd. All rights reserved.
Nasopharyngeal carcinoma, EGFR, AG1478, Cell cycle, Cell proliferation
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【期刊论文】Aloe Polysaccharides Mediated Radioprotective Effect through the Inhibition of Apoptosis
朱孝峰, Zong-Wei WANG, , Jun-Min ZHOU, Zhao-Sheng HUANG, An-Ping YANG, Zong-Chao LIU, Yun-Fei XIA, Yi-Xin ZENG and Xiao-Feng ZHU *
J. Radiat. Res., 45, 447-454(2004),-0001,():
-1年11月30日
Polysaccharides from aloe are always considered an effective radioprotector on irradiation-induced skin damage. The aim of this study was to determine if aloe polysaccharides (AP) have radioprotective effects on normal human cells in vitro and mouse survival in vivo and to explore the mechanism. Pretreatment with 50 m g/ml AP could improve the surviving fraction at 2 Gy (SF 2) of three normal cell lines 293, ECV304, and C. liver from 41.5%, 46.5%, and 40.9% to 49.4%, 72.1%, and 89.1%, respectively. AP could also reduce the apoptotic rate of C. liver cells from 9.5% and 43.0% to 2.2% and 10.9% 48 h and 72 h after 2 Gy irradiation, respectively. Western blot analysis showed that pretreatment with AP could block the upregulation of pro-apoptotic p53, Bax, and Bad and the downregulation of Bcl-2 by irradiation. AP could lower thymocyte apoptosis of mice in vivo after 6 Gy irradiation and abrogate the cell cycle perturbation. Fifty mg/kg of AP treatment for 30 min before 7.5 Gy irradiation provided the best radioprotective effect and improved the 30-day survival rate of mice to 86.0%, from 10.0%. AP exerted radioprotective effects in vitro and in vivo through an inhibition of apoptosis.
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【期刊论文】Involvement of caspase-3 activation in squamocin-induced apoptosis in leukemia cell line HL-60
朱孝峰, Xiao-Feng Zhu a, Zong-Chao Liu a, Bin-Fen Xie a, Zhi-Ming Li a, Gong-Kan Feng a, Hai-Hui Xie b, Shu-jun Wu b, Ren-Zhou Yang b, Xiao-Yi Wei b, Yi-Xin Zeng a, *
Life Sciences 70(2002)1259-1269,-0001,():
-1年11月30日
Annonaceous acetogenins have potent antitumor effect in vitro and in vivo. Squamocin is one of the annonaceous acetogenins and has been reported to have antiproliferative effect on cancer cells. Our results from this study showed that squamocin inhibited proliferation of HL-60 cells with IC 50 value of 0.17 m g/ml and induced apoptosis of HL-60 cells. Investigation of the mechanism of squamocininduced apoptosis revealed that treatment of HL-60 cells with squamocin resulted in extensive nuclear condensation, DNA fragmentation, cleavage of the death substrate poly (ADP-ribose) polymerase (PARP) and induction of caspase-3 activity. Pretreatment of HL-60 cells with caspase-3 specific inhibitor DEVD-CHO prevented squamocin-induced DNA fragmentation, PARP cleavage and cell death. The expression levels of protein bcl-2, bax have no change in response to squamocin treatment in HL-60 cells, whereas stress-activated protein kinase (SAPK/JNK) was activated after treatment with squamocin in HL-60 cells. These results suggest that apoptosis of HL-60 cells induced by squamocin requires caspase-3 activation and is related to SAPK activation. © 2002 Elsevier Science Inc. All rights reserved.
Squamocin, Apoptosis, Caspase-3, HL-60
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