王修杰
干细胞与机体老化和肿瘤发生;干细胞衰老及预防;干细胞在再生医学中的应用。
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- 姓名:王修杰
- 目前身份:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
肿瘤学
- 研究兴趣:干细胞与机体老化和肿瘤发生;干细胞衰老及预防;干细胞在再生医学中的应用。
王修杰 博士, 四川大学(华西临床医学院/医院)教授,硕、博士生导师。1988年获华西医科大学硕士学位,2004年获四川大学博士学位。1998-1999在日本东京大学分子病理学研究室高访, 研修分子肿瘤学、分子病理学、实验肿瘤学。任四川省抗癌协会常务理事、四川省诱变学会理事、四川省预防医学会毒理学专业委员会委员、《肿瘤预防与治疗》常务编委;国内多家核心期刊审稿专家,如:四川大学学报.医学版(Medline),中华微生物学与免疫学杂志,天然产物研究与开发等;国内外多家SCI期刊审稿专家,如:Acta Pharmacologica Sinica,Food Chem Toxicol, Cell Mol Neurobiol等;国家自然科学基金面上项目同行评议专家,教育部科技项目同行评议专家,四川省科技厅科技项目同行评议专家,重庆市科技项目同行评议专家等。排名第二获四川省和成都市科技进步二等奖各1项。获专利授权2项;发表科研论文100多篇,“SCI”15篇,其中第一或通讯作者10篇(总引用频次﹥100)。再生医学研究方面的科研工作为:干细胞与机体老化和肿瘤发生;干细胞衰老及预防;干细胞在再生医学中的应用。
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【期刊论文】Cytotoxicity of fig fruit latex against human cancer cells
王修杰, Jing Wang a, Xiujie Wang a, *, Shu Jiang b, Ping Lin a, Jie Zhang a, Yanrong Lu a, Qi Wang a, Zhujuan Xiong a, Yaying Wua, Jingjing Ren a, Hongliang Yang a
Food and Chemical Toxicology 46(2008)1025-1033,-0001,():
-1年11月30日
Fig fruit latex (FFL) contains significant amounts of polyphenolic compounds and can serve as a source of antioxidants after human consumption. The purpose of this study is to confirm anticancer activity of FFL against human cancer cells and to further elucidate its mechanism of activity. Human glioblastoma, hepatocellular carcinoma, and normal liver cells were used for in vitro tests of FFL effects. Those tests included cytotoxicity, colony formation inhibition, Brdu incorporation, acridine orange/ethidium bromide (AO/EB) staining for apoptotic cells, cell cycle distribution through flow cytometry (FCM), and ADP-ribosyltransferase (NAD+; poly(ADP-ribose) polymerase)-like 1 (ADPERL1) mRNA expression through RT-PCR in response to FFL treatment. After FFL treatment, the proliferation, colony formation, and Brdu labeling indices of cancer cells decreased (P<0.05), while the AO/EB stained apoptotic cells increased (P<0.05). By FCM analysis, an increase of G0/G1 phase cell population and decrease of S and G2/M phase cells were observed (P<0.01), while both ADPRTL1 mRNA expression and apoptotic indices increased (P<0.01). The findings in these studies suggested that FFL exhibited potent cytotoxicity in some human cancer cells with little effect in normal cells at certain concentration. The mechanism for such effects might be associated with the inhibition of DNA synthesis, induction of apoptosis, and cell cycle arrest of cancer cells.
Fig fruit latex, Human cancer cells, Growth inhibition, Apoptosis
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王修杰, Xiujie Wang a, *, Yuquan Wei a, Shulan Yuan a, Guanjian Liu b, Yanrong Lu Jie Zhang a, Wendong Wang c
Cancer Letters 239(2006)144-150,-0001,():
-1年11月30日
Litchi fruit pericarp (LFP) extract contains significant amounts of polyphenolic compounds, and exhibits powerful antioxidative activity against fat oxidation in vitro. The purpose of this study is to confirm the anticancer activity of LFP extract against hepatocellular carcinoma in vitro and in vivo, and to elucidate the mechanism of its activity. Human hepatocellular carcinoma cell line was tested in vitro for cytotoxicity, colony formation inhibition, and cell cycle distribution through flow cytometry after treatment with water-soluble crude ethanolic extract (CEE) from LFP. Murine hepatoma bearing-mice were fed doses of 0.15, 0.3, and 0.6 g/kg/day of water-soluble CEE in DH2O p.o. for 10 days, respectively, to test the anticancer activity and BrdU incorporation of cancer cells in vivo. LFP extract demonstrated a dose- and time-dependent inhibitory effect on cancer cell growth; IC50 was 80 mg/ml, and significantly inhibited colony formation in vitro, tumor growth and BrdU incorporation into cancer cells in vivo. The tumor inhibitory rates at doses of 0.15, 0.3, and 0.6 g/kg/day were 17.31% (PO0.05), 30.77% (P!0.05), and 44.23% (P!0.01), respectively. BrdU labeled tumor cells of treated animals were 11.80G2.79%, and were significantly lower than that in untreated controls (23.00G5.42%, P!0.05). Our findings showed that LFP extract exhibited potential anticancer activity against hepatocellular carcinoma in vitro and in vivo through proliferating inhibition and apoptosis induction of cancer cells.
Litchi fruit pericarp (, LFP), extract, Anticancer activity, Hepatocellular carcinoma, Growth inhibition, Apoptosis
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王修杰, Xiujie Wang a, *, Shulan Yuan a, Jing Wang a, Ping Lin a, Guanjian Liu b, Yanrong Lu a, Jie Zhang a, Wendong Wang c, Yuquan Wei d
Toxicology and Applied Pharmacology 215(2006)168-178,-0001,():
-1年11月30日
Litchi fruit pericarp (LFP) extract contains significant amounts of polyphenolic compounds and exhibits powerful antioxidative activity against fat oxidation in vitro. The purpose of this study is to confirm the anticancer activity of LFP extract on human breast cancer in vitro and in vivo, and to elucidate the mechanism of its activity. Human breast cancer cells were tested in vitro for cytotoxicity, colony formation inhibition, BrdU incorporation, and gene expression profiling after treatment with LFP extract. Seven nude mice bearing human breast infiltrating duct carcinoma orthotopically were tested for its anticancer activity and expression of caspase-3 in vivo by oral administration of 0.3% (0.3 mg/ml) of LFP watersoluble crude ethanolic extract (CEE) for 10 weeks. LFP extract demonstrated a dose- and time-dependent inhibitory effect on cell growth (IC50=80μg/ml), and it significantly inhibited colony formation and BrdU incorporation of human breast cancer cells. Oligonucleotide microarray analysis identified 41(1.22%) up-regulated and 129 (3.84%) down-regulated genes after LFP water-soluble CEE treatment; the predominantly up-regulated genes were involved in various biological functions including cell cycle regulation and cell proliferation, apoptosis, signal transduction and transcriptional regulation, and extracellular matrix/adhesion molecules; and down-regulated genes were mainly associated with adhesion, invasion, and malignancy of cancer cells. A 40.70% tumor mass volume reduction and significant increase of casepase-3 protein expression were observed in vivo experiment. The findings in this study suggested that LFP extract might have potential anticancer activity on both ER positive and negative breast cancers, which could be attributed, in part, to its DNA damage effect, proliferating inhibition and apoptosis induction of cancer cells through up-regulation and down-regulation of multiple genes involved in cell cycle regulation and cell proliferation, apoptosis, signal transduction and transcriptional regulation, motility and invasiveness of cancer cells; ADP-ribosyltransferase (NAD+; poly (ADP-ribose) polymerase)-like 1 (ADPRTL1), Cytochrome P450, subfamily I (CYP1A1) and Hyaluronan-mediated motility receptor (HMMR) might be the main molecular targets at which LFP water-soluble CEE acted.
Litchi fruit pericarp extract, Anticancer activity, Breast cancer, Growth inhibition, Apoptosis
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【期刊论文】Potential anticancer activity of tanshinone IIA against human breast cancer
王修杰, Xiujie Wang*, Yuquan Wei, Shulan Yuan, Guanjian Liu, Yanrong Lu, Jie Zhang and Wendong Wang
Int. J. Cancer: 116, 799-807(2005),-0001,():
-1年11月30日
Tanshinone IIA is a derivative of phenanthrene-quinone isolated from Danshen, a widely used Chinese herbal medicine. It has antioxidant properties and cytotoxic activity against multiple human cancer cell lines, inducing apoptosis and differentiation of some human cancer cell lines. Our purpose was to confirm its anticancer activity on human breast cancer in vitro and in vivo and to elucidate the mechanism of its activity. Human breast cancer cells were tested in vitro for cytotoxicity, colony formation inhibition, BrdU incorporation and gene expression profiling after treatment with tanshinone IIA. Seven nude mice bearing human breast infiltrating duct carcinoma orthotopically were tested for anticancer activity and expression of caspase-3 in vivo by s.c. injection of tanshinone IIA at a dose of 30 mg/kg 3 times/week for 10 weeks. Tanshinone IIA demonstrated a dose- and time-dependent inhibitory effect on cell growth (IC50=0.25 mg/ml), and it significantly inhibited colony formation and BrdU incorporation of human breast cancer cells. Oligonucleotide microarray analysis identified 41 upregulated (1.22%) and 24 downregulated (0.71%) genes after tanshinone IIA treatment. Upregulated genes were involved predominantly in cycle regulation, cell proliferation, apoptosis, signal transduction and transcriptional regulation; and downregulated genes were associated mainly with apoptosis and extracellular matrix/adhesion molecules. A 44.91% tumor mass volume reduction and significant increase of casepase-3 protein expression were observed in vivo. Our findings suggest that tanshinone IIA might have potential anticancer activity on both ER-positive and -negative breast cancers, which could be attributed in part to its inhibition of proliferation and apoptosis induction of cancer cells through upregulation and downregulation of multiple genes involved in cell cycle regulation, cell proliferation, apoptosis, signal transduction, transcriptional regulation, ngiogenesis, invasive potential and metastatic potential of cancer cells. ADPRTL1 might be the main target at which tanshinone IIA acted.
tanshinone IIA, anticancer activity, breast cancer, growth inhibition, apoptosis
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【期刊论文】Potential involvement of leptin in carcinogenesis of hepatocellular carcinoma
王修杰, Xiu-Jie Wang, Shu-Lan Yuan, Qing Lu, Yan-Rong Lu, Jie Zhang, Yan Liu, Wen-Dong Wang
World J Gastroenterol 2004; 10(17): 2478-2481,-0001,():
-1年11月30日
AIM: To investigate the potential involvement of leptin in carcinogenesis of hepatocellular carcinoma (HCC) and to elucidate the etiology, carcinogenesis and progress of HCC. METHODS: Expressions of Ob gene product, leptin and itsreceptor, Ob-R were investigated in 36 cases of HCC specimens and corresponding adjacent non-tumorous liver tissues with immunohistochemical staining. The effect of leptin on proliferation of Chang liver cell line and liver cancer cell line SMMC-7721 was studied with cell proliferation assay (MTT). RESULTS: Leptin expression was detected in 36 cases of adjacent non-tumorous liver tissues (36/36,100%) with moderate (++) to strong (+++) intensity; and in 72.22% (26/36) of HCC with weaker (+) intensity (P<0.05). Thirty of 36 (83.33%) cases of adjacent non-tumorous liver tissues were positive for Ob-R, with moderate (++) to strong (+++) intensity. In HCC, 11/36 (30.56%) cases were positive, with weak (+) intensity (P<0.05). In cell proliferation assay, leptin inhibited the proliferation of Chang liver cells. The cell survival rate was 10-13% lower than that of the untreated cells (P>0.05). Leptin had little effect on the proliferation of liver cancer cells (P>0.05). CONCLUSION: High level expression and decreased or absent expression of leptin and its receptor in adjacent non-tumorous liver cells and HCC cells, inhibitory effect of leptin on the proliferation of normal Chang liver cells and no effect of leptin on proliferation of liver cancer cells, may provide new insights into the carcinogenesis and progression of human HCC. It could be assumed that leptin acting as an inhibitor and/or promoter, is involved in the process of arcinogenesis and progress of human HCC.
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