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Glycogen Synthase Kinase 3β Inhibitor (2'Z,3'E)-6-Bromo-indirubin-3'-Oxime Enhances Drug Resistance to 5-Fluorouracil Chemotherapy in Colon Cancer Cells

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Chinese Journal of Cancer Research 2012年第2期24卷 116-123页

作者： Kun-ping Liu Feng Luo Si-ming Xie Li-juan Tang Mei-xiang Chen Xue-fang Wu Xue-yun Zhong Tong Zhao Department of Pathology Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China Department of Pathology Qingyuan HospitalMedical CollegeJinan UniversityQingyuan 511518China Department of Pathology Medical CollegeJinan UniversityGuangzhou 510632China Department of Pathology School of Basic Medical ScienceSouthern Medical UniversityGuangzhou 510515China

Objective： To explore the effects and mechanism of glycogen synthase kinase 3β （GSK-313） inhibitor （2＇Z,3＇E）-6-bromo-indirubin-3＇-oxime （BIO） on drug resistance in colon cancer cells. Methods： The colon cancer SW480 and SW620 cells were treated with BIO, 5-fluorouracil （5-FU） and BIO/5-FU, separately. Cell cycle distribution, apoptosis level and efflux ability of rhodamine 123 （Rh123） were detected by flow cytometry. The protein expressions of P-glycoprotein （P-gp）, multidrug resistance protein 2 （MRP2）, thymidylate synthase （TS）, β-catenin, E2F-1 and βcl-2 were detected by Western blot. β-catenin and P-gp were stained with double immunofluorescence and observed under a confocal microscope. Results： BIO up-regulated β-catenin, P-gp, MRP2 and TS, enhanced the efflux ability of Rh123, decreased Bcl-2 protein and gave the opposite effect to E2F-1 protein in SW480 and SW620 ceils. Furthermore, BIO significantly inhibited cell apoptosis, increased S and G2/M phase cells, and reduced the cell apoptosis induced by 5-FU in SW480 cells, whereas the effects were slight or not obvious in SW620 cells. Conclusion： GSK-3β was involved in drug resistance regulation, and activation of β-catenin and inhibition of E2F-1 may be the most responsible for the enhancement of 5-FU chemotherapy resistance induced by GSK-β inhibitor β10 in colon cancer.

关键词： Colorectal neoplasms Drug resistance Glycogen synthase kinase 313 Fluorouracil 13-catenin E2F-1

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Role of Lef1 in sustaining self-renewal in mouse embryonic stem cells

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Journal of Genetics and Genomics 2010年第7期37卷 441-449页

作者： Chen Huang Dajiang Qin Stem Cell and Cancer Biology Group Key Laboratory of Regenerative Biology South China Institute for Stem Cell Biology and Regenerative Medicine Guangzhou Institute of Biomedicine and Health Chinese Academy of Sciences Guangzhou 510530 China

Embryonic stem cells （ESCs） can self-renew indefinitely while maintaining the ability to generate all three germ-layer *** the importance of ESCs in developmental biology and their potential impact on regenerative medicine,the molecular mechanisms controlling ESC behavior are incompletely ***,activation of the canonical Wnt signaling pathway has been shown to contribute to mouse ESC *** we report that ectopic expression of Lef1,a component of the Wnt signaling pathway,has a positive effect on the self-renewal of mouse ***1 up-regulates Oct4 promoter activity and physically interacts with Nanog,two key components of the ESC pluripotency ***,siRNA for Lef1 induced mouse ESC *** results thus suggest that in response to Wnt signaling Lef1 binds to stabilized β-catenin and helps maintain the undifferentiated status of ESCs through modulation of Oct4 and Nanog.

关键词： embryonic stem cells Wnt signaling 13-catenin Lefl Oct4 Nanog

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Loss of Wnt5a and Ror2 protein in hepatocellular carcinoma associated with poor prognosis

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World Journal of Gastroenterology 2012年第12期18卷 1328-1338页

作者： Ming Geng Yong-Cheng Cao Ying-Jian Chen Hui Jiang Li-Quan Bi Xiao-Hong Liu Department of Pathology General Hospital of JinanMilitary Command Jinan 250031 Shandong Province China Department of Laboratory Medicine GeneralHospital of Jinan Military Command Jinan 250031 ShandongProvince China

AIM： To investigate the expression and clinical significance of Wnt member 5a （Wnt5a） and receptor tyrosine kinase-like orphan receptor 2 （Ror2） in hepatocellular carcinoma （HCC）.METHODS： In HCC tissues obtained from 85 patients, the protein expressions of Wnt5a, Rot2, 13-catenin, and Ki-67 via immunohistochemical staining using the Envision Plus System. The antibody binding was visualized with 3, 3＇-diaminobenzidine tetrahydrochloride （DAB） before brief counterstaining with Mayer＇s hematoxylin. The degree of immunohistochemical staining was recorded using a semiquantitative and subjective grading system. The mRNA expression of Rot2 was examined by real time reverse transcription polymerase chain reaction, including nineteen of the 85 HCC and three normal liver tissues. The ratios of Ror2 to the housekeeping gene GAPDH represented the normalized relative levels of Ror2 expression. To determine the prognostic factor, the outcome of the 82 patients was determined by reviewing their medical charts. The overall and diseasefree survival rates were estimated using the Kaplan-Meier method and compared with the logrank test. The prognostic analysis was carried out with univariate and multivariate Cox regressions models.RESULTS： Compared to nontumorous （hepatitis or cirrhotic） tissues, Rot2 mRNA expression was clearly decreased in HCC. Rot2 and Wnt5a protein expressions in the majority of HCC patients （63% and 77%, respectively） was significantly less in tumor tissues, as compared to adjacent nontumorous tissues, and this reduction was correlated with increasing serum α-fetoprotein and tumor stage. In 68% （58/85） of the HCC cases, the expression of IB-catenin in tumor tissues was either downregulated in the cellular membrane, upregulated in the cytoplasm, or both. Survival analysis indicated that Wnt5a and Ror2 protein expressions could be regarded as independent prognostic factors for HCC; HCC patients with decreased Wnt5a or Ror2 protein expression had a poorer progno

关键词： Hepatocellular carcinoma Wnt5a Receptortyrosine kinase-like orphan receptor 2 13-catenin Prog-nosis

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Expressions of E-cadherin, p120ctn, β-catenin and NF-κB in Ulcerative Colitis

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2015年第3期35卷 368-373页

作者：张超刘力玮孙文佳秦生辉秦灵芝王曦 Institute of Pathology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

This study was aimed to investigate the expressions of E-cadherin, p120 ctn, β-catenin and NF-κB in ulcerative colitis（UC） tissues and the implications of their expressions in the pathogenesis of UC. The expressions of E-cadherin, p120 ctn, β-catenin and NF-κB were detected by immunohistochemistry, and those of p120 ctn and NF-κB by Western blotting in 23 cases of UC and 17 cases of normal colonic tissues. The relationship between the expression of E-cadherin or NF-κB and that of p120 ctn was analyzed by Spearman rank correlation analysis. The results showed that in UC and normal colonic groups, the abnormal expression rate of E-cadherin, p120 ctn, β-catenin, and NF-κB was 52.2% vs. 0（P〈0.05）, 73.9% vs. 23.5%（P〈0.05）, 65.2% vs. 17.6%（P〈0.05） and 78.4% vs. 23.5%（P〈0.05）, respectively. p120 ctn expression was positively correlated with E-cadherin expression（r=0.404, P〈0.05）, but negatively with nuclear NF-κB expression（r= – 0.347, P〈0.05）. Western blotting showed that as compared with the normal controls, the p120 ctn protein level was significantly decreased（P〈0.05）, whereas the NF-κB protein level was increased（P〈0.05） in UC tissues. It was concluded that in the colonic tissues of UC patients, the expressions of E-cadherin, p120 ctn and β-catenin are decreased, suggesting the mucosal barrier is impaired in UC. Moreover, NF-κB is increased and activated in the UC tissues, resulting in the inflammation in UC. p120 ctn may influence the UC development through modulating intercellular adhesion and inflammatory response.

关键词： ulcerative colitis E-cadherin p120ctn 13-catenin NF-kB

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The Effect of Frat-1, Idax and Axam toward the Wnt Signaling Pathway

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Journal of Life Sciences 2011年第6期5卷 421-427页

作者： Nur Farahiyah Motiammad Reena Peter Bruce Gardiner School of Mechatronic Universiti Malaysia Perlis Perlis Arau 02600 Malaysia Melbourne School of Engineering The University of Melbourne Melbourne Victoria 3010 Australia

This paper describes the effect of Frat-1, Idax and Axam toward the Wnt signaling pathway. The Wnt pathway is an important intracellular signaling pathway that plays a crucial role in the cell cycle process at several levels of development. Understanding this pathway thoroughly will enable identification of new drug targets and thereby open avenues to more effective therapies for a range of Wnt pathway related diseases such as cancer, osteoporosis, and mesothelioma. Dishevelled （Dsh） is one of the multi-module proteins working m the Wnt pathway. The function of Dsh depends on the regulators which bind to it, components it interacts with and most importantly the Wnt signal. It is important to note that positive regulators are those factors that induce gene transcription. Conversely, the negative regulators induce β-catenin degradation. The positive regulator such as Frat- 1 would promote the Wnt signaling pathway and downstream gene transcription. Meanwhile the negative regulator such as Idax and Axam would inhibit the signaling pathway and promotes β-catenin degradation which will thereby prevent aberrant gene transcription.

关键词： Wnt signaling cellular pathway regulators 13-catenin dishevelled.

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