寿成超
个性化签名
- 姓名:寿成超
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学术头衔:
博士生导师, “973”、“863”首席科学家, 国家杰出青年科学基金获得者
- 职称:-
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学科领域:
肿瘤学
- 研究兴趣:
寿成超,男,博士学位1982年在中国医科大学本科毕业,1988年在北京医科大学研究生毕业, 1990-1994年在美国Tufts大学医学院做访问学者。 现为北京大学临床肿瘤学院生化与分子生物学研究室主任,副院长,教授,博士生导师;国家自然科学基金委员会项目专家组成员,任多个专业学术委员会副主委、常委、理事、常务理事及多种学术期刊的编委或特约审稿人。1995年获国家杰出青年科学基金资助,1997年享受国务院政府特殊津贴并入选国家百千万人材工程百千层次及北京市跨世纪学科带头人,2001年被评为北京市突出贡献专家。作为负责人先后承担了国家“863”计划、“973”计划、国家自然科学基金项目等十余项研究课题。曾在国际上率先从哺乳细胞克隆出Ras鸟核苷酸释放因子,并对其生物学活性、表达特异性、结构特点及信号传导通路等进行了一系列开拓性研究;在国内首次成功制备了具抗原内影像的抗独特型抗体,并证明了其抗原模拟作用及诱发的抗肿瘤效应;首次分别成功克隆了抗肿瘤单抗3H11与PD4的全长抗原基因,并在此基础上首次从实体瘤中分离培养获得支原体,提出了支原体感染可能与肿瘤发生相关;在国际上较早提出了肿瘤细胞中VEGF的自分泌现象,并直接证明了VEGF能刺激肿瘤细胞的增殖。在国内较早开展了以抗血管生成为策略的肿瘤生物治疗研究,获得了数个具潜在应用前景的抗血管生成小肽。以第一完成人多次获北京市科技进步一、二等奖,以第一作者或责任作者在《Nature》、《JBC》、《Oncogen》、《Sci. in Chin.》等刊物发表研究论文近七十篇,参编学术专著五部。培养毕业研究生30余名,申请国际专利2项、中国专利5项(1项已授权)。
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3397
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成果阅读
684
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成果数
13
【期刊论文】Lipoprotein p37 from Mycoplasma hyorhinis inhibiting mammalian cell adhesion
寿成超, Wen-Bin Liu†, Jian-Zhi Zhang†, Bei-Hai Jiang, Ting-Ting Ren, Man-Man Gong, Lin Meng & Cheng-Chao Shou*
Journal of Biomedical Science (2006) 13: 323-331,-0001,():
-1年11月30日
p37 protein is a membrane lipoprotein of Mycoplasma hyorhinis, and our previous work showed that there was high ratio of M. hyorhinis infection in human gastric carcinoma. To investigate the possible functions of p37 in cancer development, the nucleotide sequence of p37 gene was modified and expressed well in transfected cells. We found that p37 localized at the Golgi apparatus and could be secreted out of the cell. Human gastric cancer cells AGS, after being transfected with the p37 gene, were smaller, more spherical and easy to detach from each other. Their adhesion to matrix was also diminished and cytoskeleton in these stable p37 AGS cell was rearranged and transcription co-factor β-actin was transferred to nucleolus with down-regulation of ICAM-1 and integrin β1. These findings will be helpful for us to elucidate the effects of p37 on eukaryotic cells as well as to better understand the potential relationship between cancer and mycoplasma infection.
cell adhesion,, Golgi apparatus,, Mycoplasma hyorhinis,, p37 protein
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【期刊论文】Identification of integrin a1 as an interacting protein of protein tyrosine phosphatase PRL-3☆
寿成超, Lirong Peng, Genglin Jin, Li Wang, Jianpin Guo, Lin Meng, Chengchao Shou*
L. Peng et al./Biochemical and Biophysical Research Communications 342(2006)179-183,-0001,():
-1年11月30日
PRL-3 is a newly identified protein tyrosine phosphatase associated with tumor metastasis. It is over-expressed in various cancers, such as colorectal cancer, gastric cancer, and ovarian cancer, and is correlated with the progression and survival of cancers. Although PRL-3 plays a causative role in promoting cancer cell invasion and metastasis, the molecular mechanism is unknown. To investigate PRL-3's roles in tumorigenesis and signal transduction pathway, we screened the human placenta brain cDNA library with the bait of PRL-3 in yeast two-hybrid system. Then we identified integrin α1 as a PRL-3-interacting protein for the first time, and verified this physical association with pull-down and co-immunoprecipitation assays. Furthermore, we found that PRL-3 could down-regulate the tyrosine-phosphorylation level of integrin β1 and increased the phosphorylation level of Erk1/2. Our present discovery will provide new clues for elucidating the molecular mechanism of PRL-3 in promoting cancer invasion and metastasis.
Protein tyrosine phosphatase PRL-3, Integrin, Interaction, Erk1/, 2, Phosphorylation
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寿成超, Xiaoying Liu, Yu Sun, Jianping Guo, Hong Ma, Jiyou Li, Bin Dong, Genglin Jin, Jianzhi Zhang, Jian Wu, Lin Meng and Chengchao Shou*
Int. J. Cancer: 118, 1922-1929 (2006),-0001,():
-1年11月30日
Stem cell genetics research may be critical to our understanding of carcinogenesis, as both stem cells and cancer cells possess the ability to self-renew. Recent discoveries have indicated that the piwi family of genes plays an essential role in stem cell selfrenewal in diverse organisms. The hiwi gene, the human homolog of the piwi family, participates in germ cell proliferation and its overexpression may cause the development of germ cell malignancy, but its expression and function in epithelial solid cancers have not been explored. In the present study, we investigated whether there was an association between hiwi expression and human gastric cancer and its potential mechanism. RT-PCR findings demonstrated that hiwi was expressed in different gastric cancer cell lines. To identify the HIWI protein in gastric cancer, we developed a specific monoclonal antibody against HIWI and immunohistochemistry was performed on various gastric tissues. We found that the expression ratio of hiwi in normal gastric tissues, atrophic gastritis, intestinal metaplasia and gastric cancerswas 10% (5/50), 36% (18/50), 36% (18/50) and 76% (38/50), respectively, which was consistent with precancerous development. Notably, the expression pattern of hiwi in gastric cancer tissues was similar to that of Ki67, which was used as a marker of proliferation. Moreover, the suppression of hiwi by antisense or RNAi inhibited the growth of gastric cancer cells and induced cell cycle arrest in G2/M phase. These results suggest that hiwi may be involved in the development of gastric cancer and is a potential target for cancer therapy.
hiwi, expression, gastric cancer, proliferation
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寿成超, Beihai Jiang‡, Wenbin Liu‡, Hong Qu§, Lin Meng‡, Shumei Song‡, Tao Ouyang¶, and Chengchao Shou‡
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 280, No.6, Issue of February 11, pp. 4656-4662, 2005,-0001,():
-1年11月30日
Trastuzumab, a humanized antibody to HER-2, has been shown to be effective in the treatment of breast cancer in which HER-2 overexpression and metastasis occurs. In our search for an effective mimic epitope of HER-2 binding with trastuzumab and to develop HER-2 peptide vaccine, we screened a phage display 12-mer peptide library with trastuzumab as the target. A mimetic peptide (mimotope) H98 (LLGPYELWELSH) that could specifically recognize trastuzumab was isolated. The DNA encoding peptide H98 was cloned and expressed as the fusion protein GST-H98 in Escherichia coli BL21. The purified GST-H98 could specifically bind to trastuzumab and block the binding of trastuzumab to HER-2 protein. Moreover, H98 could significantly block the function of trastuzumab inhibiting the growth of cancer cells. Mice that were immunized with GST-H98 made specific antibody to H98 as well as to HER-2. In addition, T-cell proliferation occurred in mice immunized with GST-H98. Although no sequence homology was found between H98 and HER-2, through the use of structure analysis we were able to determine that peptide H98 contributed to a conformational epitope of HER-2. Furthermore, we determined that the last two amino acids at the C terminus, and the third together with the fourth amino acid at the N terminus of peptide H98 are critical to the binding of H98 to trastuzumab. As a result, we conclude that peptide H98 has potential for being developed as a HER-2 vaccine for biotherapy of cancer with HER-2 overexpression.
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寿成超, Ping AN, Hetian LEI, Jianzhi ZHANG, Shumei SONG, Luowen HE, Genglin JIN, Xiaoying LIU, Jian WU, Lin MENG, Meisheng LIU and Chengchao SHOU*
Int. J. Cancer: 111, 165-173 (2004),-0001,():
-1年11月30日
Although the VEGF-Flk-1-pathway has been known as the major driving force of angiogenesis, new evidence has shown that VEGFR-1/Flt-1 plays important roles during the neovascularization under pathological conditions including tumor, atherosclerosis and arthritis. In search of Flt-1 receptor antagonizing peptides, we screened a phage display 12-merpeptide library with recombinant Flt-1 protein. Seven candidate peptides were identified that specifically bound to VEGF receptor Flt-1, of which peptide F56 (WHSDMEWWYLLG) almost abolished VEGF binding to receptor Flt-1 in vitro. In vivo, F56 fused with DHFR (DHFR-F56) inhibited angiogenesis in a CAM assay. Moreover, DHFR-F56 significantly inhibited the growth of nodules of human gastric cancer cell line MGC-803 in BALB/c nude mice. Histological analyses showed that necrosis of the implanted tumor was markedly enhanced following treatment with DHFR-F56. In the severe combined immunodeficiency disease (SCID) mouse model for studying metastasis of the human breast cancer cell line BICR-H1, synthetic peptide F56 significantly inhibited tumor growth and lung metastases. Taken together, our results have demonstrated that peptide F56, as a Flt-1 receptor antagonist, fulfilled the antiangiogenic and antimetastatic effects by specifically interfering with the interaction between VEGF and receptor Flt-1. Thus, short peptide F56 may have clinical potential in tumor therapy.
tumor, angiogenesis, peptide, suppression, VEGFR-1
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【期刊论文】Subcellullar localization of tumor-associated antigen 3H11Ag
寿成超, Jianhui Guoa, Genglin Jina, Lin Menga, Hong Maa, Dezhi Niza, Jian Wua, Lan Yuanb, Chengchao Shoua, *
Biochemical and Biophysical Research Communications 324(2004)922-930,-0001,():
-1年11月30日
3H11Ag, a tumor-associated antigen defined by the monoclonal antibody 3H11 that specifically recognizes cancer cells in various tumor tissues, was successfully cloned recently, but its function is unknown. To explore the potential roles it plays in tumors, we analyzed its subcellular localization in the present study. By expressing 3H11Ag fused with fluorescent protein in COS-7 cells, we found that 3H11Ag localizes to both cytoplasm and nucleus, which was confirmed by subcellular fractionation. And sequentially extracting the nuclei of COS-7 cells transfected with 3H11Ag showed that it is a DNA- and nuclear matrix-associated protein. Moreover, by expressing a series of red fluorescent protein-tagged truncated forms of 3H11Ag, it was demonstrated that the 150 amino acid residues at its C-terminal are fully responsible for the subcellular localization. In addition, the results of the computational analysis of 3H11Ag were in accordance with those of the experimental analysis. All these data would be helpful to elucidate the functions of 3H11Ag.
Subcellular localization, 3H11Ag, BLAST, PSORT II, Coiled coil, Cell fractionation
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寿成超, LIRONG PENG, , YAN LI, LING MENG, and CHENGCHAO SHOU
HYBRIDOMA AND HYBRIDOMICS Volume 23, Number 1, 2004,-0001,():
-1年11月30日
PRL-3 is a newly identified nonclassical protein tyrosine phosphatase associated with colorectal cancer metastasis. To prepare specific monoclonal antibody (MAb) against PRL-3, cDNAs of PRL-1, -2, and -3 were cloned by RT-PCR and inserted into prokaryotic expression vector pGEX-4T1, respectively. The fusion proteins were expressed in Escherichia coli. Monoclonal antibody against PRL-3 was obtained with hybridoma technique and specific ELISA screening. Western blotting and immunohistochemistry assays showed that MAb 3B6 had specific binding ability with PRL-3 protein in eukaryotic cells. This MAb will be a helpful tool for the detection of PRL-3 protein in the tissues and serum of colorectal cancer and other cancer patients.
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寿成超, Lei Hetian‡§¶, An Ping‡¶, Song Shumei‡, Liu Xiaoying‡, He Luowen‡, Wu Jian‡, Meng Lin‡, Liu Meisheng‡, Yang Junshan§, and Shou Chengchao‡
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 277, No.45, Issue of November 8, pp. 43137-43142, 2002,-0001,():
-1年11月30日
Vascular endothelial growth factor (VEGF), one of the most important angiogenic factors, plays an essential role in both physiological and pathological angiogenesis. The VEGF receptor KDR/Flk-1 (a kinase domain receptor) mediates various biological activities of VEGF related to proliferation, differentiation, and migration of endothelial cells. Here we present a novel peptide designated K237-(HTMYYHHYQHHL), which was isolated from a phage-displayed peptide library, binding to KDR with high affinity and specificity. By interfering with the VEGF-KDR interaction, the peptide K237 inhibited proliferation of cultured primary human umbilical ein endothelial cells induced by recombinant human VEGF165 in a dose-dependent and cell type-specific manner. The peptide also exerted an anti-angiogenesis activity in vivo as revealed using the chick embryo chorioallantoic membrane angiogenesis assay. Moreover, the peptide K237 significantly inhibited the growth of solid tumors implanted beneath the breasts and their metastases to lungs in severe combined mmunodeficient mice. Taken together, these findings suggest that the peptide K237 can functionally disrupt the interaction between VEGF and the KDR receptor and cause potent biological effects that include the inhibition of angiogenesis and tumor growth. As a consequence, this peptide (and its future derivatives) may have use as a potential cancer therapy.
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【期刊论文】Mycoplasma infections and different human carcinomas
寿成超, Su Huang, Ji You Li, Jan Wu, Lin Meng and Cheng Chao Shou
World J Gastroentero, 2001; 7 (2): 266-269,-0001,():
-1年11月30日
ifferent paraffin embedded carcinoma tissues with immunohistochemistry. PCR was applied to amplify the mycoplasma DNA from the positive samples for confirming immunohistochemistry. RESULTS Fifty of 90 cases (56%) of gastric carcinoma were positive for mycoplasma hyorhinis. In other gastric diseases, the mycoplasma infection ratio was 28% (18/49) in chronic superficial gastritis, 30% (14/46) in gastric ulcer and 37% (18/49) in intestinal metaplasia. The difference is significant with gastric cancer (χ2=12.06, P<0.05). In colon carcinoma, the mycoplasma infection ratio was 55.1% (32/58),but it was 20.9% (10/49) in adenomarous polyp (χ2 = 13.46, P<0.005). Gastric and colon cancers with high differentiation had a higher mycoplasma infection ratio than those with low differentiation (P<0.05). Mycoplasma infection in esophageal cancer, lung cancer, breast cancer and glioma was 50.9% (27/53), 52.6% (31/59), 39.7% (25/63)and 41% (38/91), respectively. The mycoplasma DNA was successfully amplified with the DNA extracted from the cancer tissues that were positive for mycoplasma infection (detected with antibody PD4). CONCLUSION There was high correlation between mycoplasma infection and different cancers, which suggests the possibility of an association between the two. The mechanism involved in oncogenesis by mycoplasma remains unknown.
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寿成超, Xuejun Tian, *, , Shumei Song, Jian Wu, Lin Meng, Zhiwei Dong, †, and Chengchao Shou*
Biochemical and Biophysical Research Communications 286, 505-512 (2001),-0001,():
-1年11月30日
Vascular endothelial growth factor (VEGF) is known to be a highly specific mitogen for endothelial cells through two high-affinity tyrosine kinase receptors, VEGFR-1 and VEGFR-2, which are almost specifically expressed in endothelial cells. However, recent findings showed that VEGF receptors may also expressed by nonendothelial cells, especially by tumor cells. To further understand the functional expression of VEGF receptors by nonendothelial cells, our preliminary screening detected the expression of VEGFR-2 in 115 different paraffin-embedded cancer specimens including 35 cases of bladder tumor, 30 cases of breast cancer, 25 cases of intestinal cancer, and 25 cases of lung cancer with immunohistochemistry. The results showed that VEGFR-2 was widely expressed in different tumor tissues. By reverse transcription PCR, NCIH23, NCI-H460, MGC803, MDA-MB-231, 293, and MCF7 cells were evaluated for the mRNA expression of both VEGF and VEGFR-2. The data indicated that all these tumor cell lines expressed detectable amounts of VEGF mRNA, but only 293, MCF7, and MGC803 cells coexpressed VEGFR-2. Immunoblot analysis also demonstrated the expression of VEGFR-2 at protein level. We further demonstrate that exogenous rhVEGF165 could stimulate cell growth in MGC803, a tumor cell line derived from gastric adenocarcinoma, in a doseand time-dependent manner. Furthermore, the antibodies against rhVEGF165 and VEGFR-2 could block rhVEGF165-mediated proliferation of MGC803 cells. These unexpected results provided direct evidence that VEGF may act as an autocrine growth factor to induce the proliferation of gastric adenocarcinoma cells as well as tumor angiogenic cells, thus suggesting a promising tumor therapeutic application based upon the VEGF system.
tumor, VEGF,, VEGFR-2, stimulation.,
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