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Aminoguanidine impedes human pancreatic tumor growth and metastasis development in nude mice

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World Journal of Gastroenterology 2009年第9期15卷 1065-1071页

作者： Nora A Mohamad Graciela P Cricco Lorena A Sambuco Máximo Croci Vanina A Medina Alicia S Gutiérrez Rosa M Bergoc Elena S Rivera Gabriela A Martín Laboratory of Radioisotopes School of Pharmacy and BiochemistryUniversity of Buenos AiresJunín 954 (C1113AAB)Buenos AiresArgentina Institute of Immunooncology Dr. Ernesto Crescenti Av. Córdoba 3200 (C1187AAS)Buenos AiresArgentina National Research Council (CONICET) Av. Rivadavia 1917 (C1033AAJ)Buenos AiresArgentina

AIM:To study the action of aminoguanidine on pancreatic cancer xenografts in relation to cell proliferation,apoptosis,redox status and ***:Xenografts of PANC-1 cells were developed in nude mice. The animals were separated into two groups:control and aminoguanidine treated. tumor growth,survival and appearance of metastases were determined in vivo in both groups. tumors were excised and ex vivo histochemical studies were performed. Cell growth was assessed by Ki-67 expression. Apoptosis was studied by intratumoral expression of B cell lymphoma-2 protein (Bcl-2) family proteins and Terminal deoxynucleotidyl transferase biotin-dUTP Nick End Labeling (Tunel). Redox status was evaluated by the expression of endothelial nitric oxide synthase (eNOS),catalase,copper-zinc superoxide dismutase (CuZnSOD),manganese superoxide dismutase (MnSOD) and glutathione peroxidase (GPx). Finally,vascularization was determined by Massons trichromic staining,and by VEGF and CD34 ***:tumor volumes after 32 d of treatment by aminoguanidine (AG) were significantly lower than in control mice (P tumoral vascularization (trichromic stain) and the expression of Ki-67,Bax,eNOS,CD34,VEGF,catalase,CuZnSOD and MnSOD were diminished in AG treated mice (P tumoral action of aminoguanidine is associated with decreased cell proliferation,reduced angiogenesis,and reduced expression of antioxidant enzymes.

关键词： Aminoguanidine Pancreatic ductal carcinoma tumor growth Metastasis Apoptosis

ADENOVIRUS-MEDIATED EXPRESSION OF PEX, A NONCATALYTIC FRAGMENT OF MATRIX METALLOPROTEINASE-2, AND IT’S INHIBITION ON ANGIOGENESIS AND tumor growth

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Chinese Journal of Cancer Research 2006年第1期18卷 12-18页

作者：李金萍胡颖林仲翔张志谦 Department of Cell Biology Beijing Institute for Cancer Research Peking University School of Oncology Beijing 100036

Objective： To develop an adenovirus system to deliver biologically active peptides or proteins such as angiogenesis inhibitors in vivo for the treatment of cancer. Methods： DNA recombination techniques were employed to construct adenovirus shuttle vector, in which angiogenesis inhibitor was put downstream of rat growth hormone signal peptide, and the C-terminal was the myc-epitope 10-amino-acid peptide for the following up of the protein. Adenovirus was made using the bacteria recombination method. We tested this system using an angiogenesis inhibitor chick MMP-2 C-terminal hemopexin-like fragment （PEX） in Sarcoma 180 （S-180） bearing Kunming mice. The anti-angiogenie effect was performed by chick chorioallantoic membrane assay. Results： PEX was readily secreted outside human stomach carcinoma BGC823 cells as demonstrated by immunofluorcscent staining and western blot infected by adenovirus with rat growth hormone signal peptide （E-T-rGH-PEX）. However, without signal pcptide （E-T-PEX）, PEX was expressed and localized in the cytoplasm of the infected cells, and formed large aggregates, which suggested that PEX was insoluble. The adenovirus E-T-rGH-PEX could inhibit angiogenesis, while E-T-rGH-PEX not. The adenoviruses of E-T-rGH-PEX inhibited the growth of S-180 tumor significantly compared with the empty virus control group E-T （P=0.026） and without signal peptide group E-T-PEX （P=0.006） respectively, while E-T-PEX had little effect. Conelusion： These results suggest that this adenoviral system is likely to be used in the gene therapy of cancer to deliver angiogenesis inhibitors.

关键词： MMP-2 PEX CAM Angiogenesis tumor growth

Analysis of a Free Boundary Problem Modeling tumor growth

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Acta Mathematica Sinica,English Series 2005年第5期21卷 1071-1082页

作者： Shang Bin CUI (Shangbin CUI) Institute of Mathematics Sun Yat-Sen University Guangzhou 510275 P. R. China

In this paper, we study a free boundary problem arising from the modeling of tumor growth. The problem comprises two unknown functions： R = R（t）, the radius of the tumor, and u = u（r, t）, the concentration of nutrient in the tumor. The function u satisfies a nonlinear reaction diffusion equation in the region 0 〈 r 〈 R（t）, t 〉 0, and the function R satisfies a nonlinear integrodifferential equation containing u. Under some general conditions, we establish global existence of transient solutions, unique existence of a stationary solution, and convergence of transient solutions toward the stationary solution as t →∞.

关键词： Free boundary problem tumor growth Global solution Asymptotic behavior

miR-205 is frequently downregulated in prostate cancer and acts as a tumor suppressor by inhibiting tumor growth

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Asian Journal of Andrology 2013年第6期15卷 735-741,I0005页

作者： Ning Wang Qi Li Ning-Han Feng Gong Cheng Zhao-Long Guan Yang Wang Chao Qin Chang-Jun Yin Li-Xin Hua Department of Urology First Affiliated Hospital of Nanjing Medical University Nanjing 210029 China

The purpose of this study was to elucidate the molecular mechanisms of microRNA-205 （miR-205） as a tumor suppressor in prostate cancer （PCa）o In the present study, microRNA microarray analysis suggested that the expression of miR-205 was significantly decreased in advanced PCa compared with early PCa. Real-time PCR analysis also indicated that miR-205 expression was significantly decreased in PCa tissues compared with non-cancerous tissues. Moreover, the expression of miR-205 has been demonstrated to be associated with the clinicopathological stage and total/free prostate-specific antigen （PSA） level of PCa. Functional analyses showed that both the overexpression of miR-205 and the knockdown of c-SRC in PCa cell lines could inhibit cell growth, colony formation, migration, invasion and the cell cycle as well as induce cell apoptosis in vitro. Furthermore, over-expressing miR-205 reduced tumorigenicity in vivo. Through a luciferase activity assay and Western blotting, c-SRCwas identified as a target of miR-205 in cells. The overexpression of miR-205 suppressed c-SRC and its downstream signaling molecules, including FAK, p-FAK, ERK1/2 and D-ERK1/2, and attenuated cell proliferation, invasion and tumor growth.

关键词： c-SRC miR-205 prostate cancer (PCa) tumor growth

Hybrid discrete-continuum model of tumor growth considering capillary points

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Applied Mathematics and Mechanics(English Edition) 2013年第10期34卷 1237-1246页

作者：吕杰许世雄姚伟周瑜龙泉 Department of Medical Instrumentation Engineering Shanghai Medical Instrumentation College Department of Mechanics and Engineering Science Fudan University Neusoft Medical System Brunel Institute for Bioengineering School of Engineering and DesignBrunel UniversityUxbridge Middlesex UB8 3PH U. K

A hybrid discrete-continuum model of tumor growth in the avascular phase considering capillary points is established. The influence of the position of capillary points on tumor growth is also studied by simulation. The results of the dynamic tumor growth and the distribution of oxygen, matrix-degrading enzymes, and extracellular matrixconcentration in the microenvironment with respect to time are shown by graphs. The relationships between different oxygenated environments and the numbers of surviving, dead, proliferative, and quiescent tumor cells are also investigated.

关键词： mathematical model capillary point tumor growth oxygen

Numerical simulation of avascular tumor growth based on p27 gene regulation

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Applied Mathematics and Mechanics(English Edition) 2013年第3期34卷 327-338页

作者： Yu ZHOU Jia-wan CHEN Xiao-ning DAI Yan CAI Wei YAO Shi-xiong XU Quan LONG Department of Mechanics and Engineering Science Fudan University Shanghai 200433 P. R. China Brunel Institute for Bioengineering Brunel University Uxbridge Middlesex UB8 3PH United Kingdom

A multi-scale continuous-discrete model based on the effects of the p27 gene control is built to simulate the avascular tumor growth. At the tissue level, the continuous Eulerian model is adopted to determine the distribution of the concentration of oxygen, the extracellular matrix （ECM）, and the matrix-degradative enzyme （MDE）. At the cellular level, the discrete Lagrangien model is adopted to determine the movement, the proliferation, and the death of single tumor cells （TCs）. At the genetic level, whether a cell is committed to mitosis is determined by solving a set of equations modeling the effects of the p27 gene control. The avascular morphological evolution of the solid tumor growth is simulated, including the radius the oxygen distribution over time, and the expression. of the solid tumor, the number of the TCs, inhibiting effect＇ of the up-regulating p27 gene

关键词： tumor growth avascular p27 gene multi-scale continuous-discrete model,numerical simulation

Composite Waves for a Cell Population System Modeling tumor growth and Invasion

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Chinese Annals of Mathematics,Series B 2013年第2期34卷 295-318页

作者： Min TANG Nicolas VAUCHELET Ibrahim CHEDDAD Irene VIGNON-CLEMENTEL Dirk DRASDO Benoit PERTHAME Department of mathematics Institute of Natural Sciences and MOE-LSCShanghai Jiao Tong University INRIA Paris Rocquencourt ParisFrance Laboratoire Jacques-Louis Lions UPMC Univ Paris 06 and CNRS UMR 7598F-75005ParisFrance

In the recent biomechanical theory of cancer growth,solid tumors are considered as liquid-like materials comprising elastic *** this fluid mechanical view,the expansion ability of a solid tumor into a host tissue is mainly driven by either the cell diffusion constant or the cell division rate,with the latter depending on the local cell density(contact inhibition) or/and on the mechanical stress in the *** the two by two degenerate parabolic/elliptic reaction-diffusion system that results from this modeling,the authors prove that there are always traveling waves above a minimal speed,and analyse their *** appear to be complex with composite shapes and *** small parameters allow for analytical solutions,and in particular,the incompressible cells limit is very singular and related to the Hele-Shaw *** singular traveling waves are recovered numerically.

关键词： Traveling waves Reaction-diffusion tumor growth Elastic material

A Deep Look into the Program of Rapid tumor growth of Hepatocellular Carcinoma

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Journal of Clinical and Translational Hepatology 2021年第1期9卷 22-31页

作者： Jie Wang Yi Lou Jianmin Lu Yuxiao Luo Anqian Lu Anna Chen Jiantao Fu Jing Liu Xiang Zhou Jin Yang Department of Translational Medicine Affiliated Hospital of Hangzhou Normal UniversityInstitute of Hepatology and Metabolic Diseases of Hangzhou Normal UniversityHangzhou Normal UniversityHangzhouZhejiangChina Department of Liver Disease Affiliated Hospital of Hangzhou Normal UniversityHangzhou Normal UniversityHangzhouZhejiangChina Department of Occupational Medicine Hangzhou Red Cross HospitalZhejiang Provincial Integrated Chinese and Western Medicine HospitalHangzhouZhejiangChina Department of Orthopedics Affiliated Hospital of Hangzhou Normal UniversityHangzhou Normal UniversityHangzhouZhejiangChina

Background and Aims:Great efforts have been made towards increasing our understanding of the pathogenesis involved in hepatocellular carcinoma(HCC),but the rapid growth inherent to such tumor development remains to be ***:We identified distinct gene coexpression modes upon liver tumor growth using weighted gene coexpression network *** of tumor growth as signaling activity was employed to understand the main cascades responsible for the *** genes in the modules were determined,examined in vitro,and further assembled into the growth ***:We revealed modules related to the different growth states in HCC,especially the fastest growth module,which is preserved among different HCC ***,signaling flux in the cell cycle pathway was found to act as a driving force for rapid *** hub genes in the module were identified and assembled into the growth signature,and two genes(NCAPH,and RAD54L)were tested for their growth potential in *** alteration of the growth signature affected the global gene *** activity of the signature was associated with tumor metabolism and immunity in ***,the prognosis effect of the growth signature was reproduced in nine ***:These results collectively demonstrate the molecule organization of rapid tumor growth in HCC,which is a highly synergistic process,with implications for the future management of patients.

关键词： Hepatocellular carcinoma tumor growth Coexpression network Cell cycle Metabolism

Knockdown of DEAD-box 51 inhibits tumor growth of esophageal squamous cell carcinoma via the PI3K/AKT pathway

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World Journal of Gastroenterology 2022年第4期28卷 464-478页

作者： Dong-Xin Hu Qi-Feng Sun Lin Xu Hong-Da Lu Fan Zhang Zhen-Miao Li Ming-Yan Zhang Department of Thoracic Surgery Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250000Shandong ProvinceChina Department of Gastroenterology Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250000Shandong ProvinceChina

BACKGROUND Esophageal squamous cell carcinoma(ESCC)is one of the most prevalent malignancies that seriously threaten people’s health ***-box helicase 51(DDX51)is a member of the DEAD-box(DDX)RNA helicase family,and drives or inhibits tumor progression in multiple cancer *** To determine whether DDX51 affects the biological behavior of *** The expression of DDX51 in ESCC tumor tissues and adjacent normal tissues was detected by Immunohistochemistry(IHC)analyses and quantitative PCR(qPCR).We knocked down DDX51 in ESCC cell lines by using a small interfering RNA(siRNA)*** proliferation,apoptosis,and mobility of DDX51 siRNAtransfected cells were *** effect of DDX51 on the phosphoinositide 3-kinase(PI3K)/AKT pathway was investigated by western blot analysis.A mouse xenograft model was established to investigate the effects of DDX51 knockdown on ESCC tumor *** DDX51 exhibited high expression in ESCC tissues compared with normal tissues and represented a poor prognosis in patients with *** of DDX51 induced inhibition of ESCC cell proliferation and promoted ***,DDX51 siRNA-expressing cells also exhibited lower migration and invasion *** into the underlying mechanisms suggested that DDX51 knock down induced inactivation of the PI3K/AKT pathway,including decreased phosphorylation levels of phosphate and tensin homolog,PI3K,AKT,and mammalian target of *** experiments demonstrated that the AKT activator insulin-like growth factor 1 could reverse the inhibitory effects of DDX51 on ESCC malignant ***,we injected DDX51 siRNA-transfected TE-1 cells into an animal model,which resulted in slower tumor *** Our study suggests for the first time that DDX51 promotes cancer cell proliferation by regulating the PI3K/AKT pathway;thus,DDX51 might be a therapeutic target for ESCC.

关键词： Esophageal squamous cell carcinoma DDX51 PI3K/AKT pathway tumor growth Therapeutic target