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15-PGDH is reduced and induces apoptosis and cell cycle arrest in gastric carcinoma

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World Journal of Gastroenterology 2012年第10期18卷 1028-1037页

作者： Li-Hong Lou Da-Dao Jing Yue-Xing Lai Ying-Ying Lu Ji-Kun Li Kai Wu International Medical Care Center Shanghai First People＇s Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200080 China Department of Gastroenterology Shanghai First People＇s Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200080 China Department of Surgery Shanghai First People＇s Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200080 China

AIM: To investigate the expression of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in human gastric cancer and it's mechanism in apoptosis and cell cycle arrest. METHODS: Expression of 15-PGDH mRNA and protein was examined by immunohistochemistry, immunocytochemistry, reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting in tissue from human gastric cancer, gastric precancerous state (gastric polyps and atrophic gastritis), normal stomach, and gastric cancer cell lines. The relationship between gastric cancer, gastric precancerous state and 15-PGDH expression was determined. The association between expression of 15-PGDH and various clinicopathological parameters in gastric cancer was evaluated. Human gastric cancer cell line SGC-7901 was transfected with 15-PGDH expression plasmids. The effect of 15-PGDH on the cell cycle was examined by flow cytometry. The effect of 15-PGDH on apoptosis was examined by transmission electron microscopy, flow cytometry and transferasemediated nick end labeling (TUNEL) assay. Expression of cell cycle (p21, p27, p16 and p53) and apoptosis (Survivin, BCL-2, BCL-XL, BAK and BAX) genes was analyzed by RT-PCR. RESULTS: Expression of 15-PGDH mRNA and protein in human gastric cancer tissues was significantly lower than in normal gastric tissues (P < 0.01). Expression in human gastric cancer cell lines MKN-28 and MKN-45 was reduced, and absent in SGC-7901 cells (P < 0.05). Reduction of 15-PGDH expression was also found in precancerous tissues, such as gastric polyps and atrophic gastritis (P < 0.01). There was a significant difference in expression of 15-PGDH among various gastric cancer pathological types (P < 0.05), with or without distant metastasis (P < 0.05) and different TNM stage (P < 0.01). Flow cytometry demonstrated a significant increase in apoptotic cells in SGC-7901 cells transfected with pcDNA3/15-PGDH plasmid for 24 and 48 h (P < 0.01), and an increased fraction of sub-G1 phase after transfection (P <

关键词： Gastric carcinoma 15-hydroxyprostaglandin dehydrogenase Apoptosis Cell cycle arrest tumor growth

Therapeutic implications of cancer stem cells in prostate cancer

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Cancer Biology & Medicine 2023年第6期20卷 401-420页

作者： Pinaki Banerjee Prachi Kapse Shehnaz Siddique Moumita Kundu Jasoda Choudhari Varshasnata Mohanty Diksha Malhotra Suresh W.Gosavi Rajesh N.Gacche Gopal C.Kundu National Centre for Cell Science Savitribai Phule Pune University CampusPune 411007India School of Basic Medical Science Savitribai Phule Pune UniversityPune 411007India School of Biotechnology KIIT Deemed to be UniversityBhubaneswar 751024India Department of Biotechnology Savitribai Phule Pune UniversityPune 411007IndiaSchool of BiotechnologyKIIT Deemed to be UniversityBhubaneswar 751024India Kalinga Institute of Medical Sciences(KIMS) KIIT Deemed to be UniversityBhubaneswar 751024India

Prostate cancer, one of the most frequently occurring cancers in men, is a heterogeneous disease involving multiple cell types within tumors. This tumor heterogeneity at least partly results from genomic instability leading to sub-clonal cellular differentiation. The differentiated cell populations originate from a small subset of cells with tumor-initiating and stem-like properties. These cells, termed prostate cancer stem cells(PCSCs), play crucial roles in disease progression, drug resistance, and relapse. This review discusses the origin, hierarchy, and plasticity of PCSCs;methods for isolation and enrichment of PCSCs;and various cellular and metabolic signaling pathways involved in PCSC induction and maintenance, as well as therapeutic targeting.

关键词： Epithelial-mesenchymal transition metastasis prostate cancer cancer stem cells tumor growth tumor microenvironment signaling

FORMATION OF NECROTIC CORES IN THE growth OF tumorS: ANALYTIC RESULTS

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Acta Mathematica Scientia 2006年第4期26卷 781-796页

作者：崔尚斌 Department of Mathematics Zhongshan University Guangdong 510275China

In this article, the author studies the mechanism of formation of necrotic cores in the growth of tumors by using rigorous analysis of a mathematical model. The model modifies a corresponding tumor growth model proposed by Byrne and Chaplain in 1996, in the case where no inhibitors exist. The modification is made such that both necrotic tumors and nonnecrotic tumors can be considered in a joint way. It is proved that if the nutrient supply is below a threshold value, then there is not dormant tumor, and all evolutionary tumors will finally vanish. If instead the nutrient supply is above this threshold value then there is a unique dormant tumor which can either be necrotic or nonnecrotic, depending on the level of the nutrient supply and the level of dead-cell dissolution rate, and all evolutionary tumors will converge to this dormant tumor. It is also proved that, in the *** case, if the dormant tumor is necrotic then an evolutionary tumor will form a necrotic core at a finite time, and if the dormant tumor is nonnecrotic then an evolutionary tumor will also be nonnecrotic from a finite time.

关键词： tumor growth necrotic core formation asymptotic behavior stability

Analysis of a System Describing Proliferative-Quiescent Cell Dynamics

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Chinese Annals of Mathematics,Series B 2018年第2期39卷 345-356页

作者： Jean CLAIRAMBAULT Benoit PERTHAME Andrada Quillas MARAN Dedicated to Philippe G. Ciarlet on the occasion of his 80th birthda

Systems describing the dynamics of proliferative and quiescent cells are commonly used as computational models, for instance for tumor growth and *** on the very earliest stages of hematopoiesis, stem cells and early progenitors, the authors introduce a new method, based on an energy/Lyapunov functional to analyze the long time behavior of solutions. Compared to existing works, the method in this paper has the advantage that it can be extended to more complex situations. The authors treat a system with space variable and diffusion, and then adapt the energy functional to models with three equations.

关键词： Stability analysis Lyapunov functional Energy method Parabolic sys-tems Proliferative and quiescent cells tumor growth Hematopoiesis

Analysis of the role of dihydromyricetin derived from vine tea(Ampelopsis grossedentata)on multiple myeloma by activating STAT1/RIG-I axis

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Oncology Research 2024年第8期32卷 1359-1368页

作者： WEI JIANG MEI ZHOU Department of Hematology Shaoxing Shangyu People’s HospitalShaoxing312000China Department of Hematology Zhuji People’s HospitalShaoxing311800China

Multiple myeloma(MM)is a plasma cell malignancy and remains incurable as it lacks effective curative approaches;thus,novel therapeutic strategies are desperately *** study aimed to explore the therapeutic role of dihydromyricetin(DHM)in MM and explore its *** MM and normal plasma samples,human MM cell lines,and normal plasma cells were used for in vitro *** counting kit-8(CCK-8),flow cytometry,and trans-well assays were performed for the assessment of cell viability,apoptosis,migration,and invasion,*** real-time polymerase chain reaction(qRT-PCR)was employed to assess the mRNA expression of signal transducer and activator of transcription 1(STAT1)and retinoic acid-inducible gene I(RIG-I).Western blotting was employed to assess E-cadherin,N-cadherin,signal transducer,STAT1,p-STAT1,and RIG-I protein expression.A tumor xenograft model was used for in vivo ***,dihydromyricetin(DHM)dose-dependently restrained viability,apoptosis,migration,and invasion,and facilitated apoptosis of U266 *** DHM treatment,the Ecadherin level was increased and the N-cadherin level was decreased in U266 and RPMI-8226 cells,suggesting the inhibitory effects of DHM on epithelial-mesenchymal transition(EMT)in ***,the levels of p-STAT1/STAT1 and RIG-I were down-regulated in ***,the STAT1 inhibitor fludarabine undid the suppressive effect of DMH on the malignant characteristics of U266 ***,DHM inhibited MM tumor growth and EMT,and activated STAT1/RIG-I pathway in ***,this study first revealed that DHM can restrain EMT and tumor growth in MM by activating STAT1/RIG-I signaling,which provides a novel drug for the treatment of MM.

关键词： Dihydromyricetin Multiple myeloma Epithelial-mesenchymal transition tumor growth

Norcantharidin inhibits growth of human gallbladder carcinoma xenografted tumors in nude mice by inducing apoptosis and blocking the cell cycle in vivo

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Hepatobiliary & Pancreatic Diseases International 2010年第4期9卷 414-422页

作者： Fan, Yue-Zu Zhao, Ze-Ming Fu, Jin-Ye Chen, Chun-Qiu Sun, Wei Tongji Univ Sch Med Tongji Hosp Dept Surg Shanghai 200065 Peoples R China Shanghai Jiao Tong Univ Peoples Hosp 9 Dept Surg Shanghai 200065 Peoples R China

BACKGROUND: Gallbladder carcinoma, a lethal malignant neoplasm with poor prognosis, has dismal results of surgical resection and chemoradiotherapy. We previously reported that norcantharidin (NCTD) is useful against growth, proliferation, and invasion of human gallbladder carcinoma GBC-SD cells in vitro. In this study, we further studied the inhibitory effect of NCTD on the growth of xenografted tumors of human gallbladder carcinoma in nude mice in vivo and the underlying mechanisms. METHODS: The tumor xenograft model of human gallbladder carcinoma in nude mice in vivo was established with subcutaneous GBC-SD cells. The experimental mice were randomly divided into control, 5-FU, NCTD, and NCTD+5-FU groups which were given different treatments. tumor growth in terms of size, growth curve, and inhibitory rate was evaluated. Cell cycle, apoptosis, and morphological changes of the xenografted tumors were assessed by flow cytometry and light/electron microscopy. The expression of the cell cycle-related proteins cyclin-D1 and p27 as well as the apoptosis-related proteins Bcl-2, Box, and survivin were determined by the streptavidin-biotin complex (SABC) method and RT-PCR. RESULTS: NCTD inhibited the growth of the xenografted tumors in a dose- and time-dependent manner. tumor volume decreased (5.61+/-0.39 vs. 9.78+/-0.61 cm(3), P=0.000) with an increased tumor inhibitory rate (42.63% vs. 0%, P=0.012) in the NTCD group compared with the control group. The apoptosis rate increased (15.08+/-1.49% vs. 5.49+/-0.59%, P=0.0001) along with a decreased percentage of cells in S phase (43.47+/-2.83% vs. 69.85+/-1.96%, P=0.0001) in the NTCD group compared with the control group. The morphological changes of apoptosis such as nuclear shrinkage, chromatin aggregation, chromosome condensation, and typical apoptosis bodies in the xenografted tumor cells induced by NCTD were observed by light and electron microscopy. The expression of cyclin-D1, Bcl-2 and survivin proteins/mRNAs decreased s

关键词： norcantharidin gallbladder neoplasm tumor growth apoptosis cell cycle

Tet methylcytosine dioxygenase 2 suppresses renal cell cancer proliferation and metastasis by regulating the miR-200c-SCD axis

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BIOCELL 2021年第3期45卷 599-615页

作者： BENJIANG QIAN YOUFENG HUANG ZHENQIANG QIU XIAOYAN YING GUANG YANG HUIZHANG LI JIANMING TAN Fujian Provincial Key Laboratory of Transplant Biology Department of UrologyDongfang Hospital(900 Hospital of the Joint Logistics Team)School of MedicineXiamen UniversityFuzhou350025China Institute of Ningde Urological Research and Department of Urology Affiliated Mindong Hospital of Fujian Medical UniversityFu’an355000China Department of Neurology Affiliated Mindong Hospital of Fujian Medical UniversityFu’an355000China

Tet methylcytosine dioxygenase 2(TET2)acts as an antioncogene that is investigated in different *** the effects of TET2 in renal cell cancer(RCC)is still known ***,quantitative real-time PCR(qRT-PCR),Western blot,and immunofluorescence were performed to exam gene and protein *** proliferation was measured using Cell Counting Kit-8(CCK-8).Transwell assay was performed to detect cell metastasis *** cytometry was performed to analyze the cell cycle and cell *** effects of TET2 on RCC growth in vivo was analyzed using a mouse xenograft *** found that TET2 and miR-200c were decreased in RCC tissues,and hypermethylation of miR-200c promoter was *** of TET2 promoted miR-200c expression by reducing miR-200c promoter ***,overexpression of TET2 or miR-200c suppressed cell growth and ***,knockdown of miR-200c could moderate TET2 mediated cell growth ***,we found miR-200c directly regulates Stearoyl-CoA desaturase(SCD)gene ***,in vivo experiment results confirmed that TET2 inhibited tumor *** conclusion,TET2 acts as an antioncogene in RCC by regulating the miR-200c-SCD axis and providing a potential target for RCC diagnosis and treatment.

关键词： TET2 miR-200c SCD Renal cell cancer tumor growth

Time delays in proliferation process for solid avascular tumor under the action of external inhibitors

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International Journal of Biomathematics 2015年第2期8卷 77-89页

作者： Shihe Xu Meng Bai School of Mathematics and Statistics Zhaoqing University Zhaoqing 526061 P. R. China

In this paper a delayed mathematical model for tumor growth under the action of external inhibitors is studied. The delay represents the time taken for cells to undergo mitosis. External inhibitor means that an inhibitor is either developed from the immune system of the body or administered by medical treatment to distinguish with that secreted by tumor itself. Non-negativity of solutions is studied. Local and global stabilities of the stationary solutions are proved for some parameter values. The analysis of the effect of inhibitor＇s parameters on tumor＇s growth is presented. The results show that dynamical behavior of solutions of this model is similar to that of solutions for corresponding nondelayed model for some parameter values.

关键词： tumor growth inhibitors time delay local stability global stability.

Controversies regarding transplantation of mesenchymal stem cells

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World Journal of Transplantation 2024年第2期14卷 48-61页

作者： Tsvetelina Velikova Tereza Dekova Dimitrina Georgieva Miteva Department of Medical Faculty Sofia University St.Kliment OhridskiSofia 1407Bulgaria Department of Genetics Faculty of BiologySofia University St.Kliment OhridskiSofia 1164Bulgaria

Mesenchymal stem cells(MSCs)have tantalized regenerative medicine with their therapeutic potential,yet a cloud of controversies looms over their clinical *** comprehensive review navigates the intricate landscape of MSC controversies,drawing upon 15 years of clinical experience and *** delve into the fundamental properties of MSCs,exploring their unique immuno-modulatory capabilities and surface *** heart of our inquiry lies in the controversial applications of MSC transplantation,including the perennial debate between autologous and allogeneic sources,concerns about efficacy,and lingering safety ***,we unravel the enigmatic mechanisms surro-unding MSC transplantation,such as homing,integration,and the delicate balance between differentiation and paracrine *** also assess the current status of clinical trials and the ever-evolving regulatory *** we peer into the future,we examine emerging trends,envisioning personalized medicine and innovative delivery *** review provides a balanced and informed perspective on the controversies,offering readers a clear understanding of the complexities,challenges,and potential solutions in MSC transplantation.

关键词： Mesenchymal stem cells Transplantation controversies Regenerative medicine Autoimmune diseases Chronic inflammatory illnesses tumor growth Metastasis Therapeutic potential Clinical use of mesenchymal stem cell