Mesenchymal Stem Cells Directly Interact with Breast Cancer Cells and Promote Tumor Cell Growth In Vitro and In Vivo

2013 ◽  
Vol 22 (23) ◽  
pp. 3114-3127 ◽  
Author(s):  
Katharina Mandel ◽  
Yuanyuan Yang ◽  
Axel Schambach ◽  
Silke Glage ◽  
Anna Otte ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Growth ◽  
Tumor Cell ◽  
Breast Cancer Cells ◽  
Tumor Cell Growth ◽  
Promote Tumor Cell

Human mesenchymal stem cells play a dual role on tumor cell growth in vitro and in vivo

2011 ◽  
Vol 226 (7) ◽  
pp. 1860-1867 ◽  
Author(s):  
Lin Li ◽  
Hui Tian ◽  
Weiming Yue ◽  
Feng Zhu ◽  
Shuhai Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Growth ◽  
Tumor Cell ◽  
Human Mesenchymal Stem Cells ◽  
Dual Role ◽  
Tumor Cell Growth

scholarly journals The in vitro and in vivo effects of mesenchymal stem cells on breast cancer cells

2017 ◽  
Vol 28 ◽  
pp. i15
Author(s):  
T. Herheliuk ◽  
O. Perepelytsina ◽  
O. Yakymchuk ◽  
L. Ostapchenko ◽  
M. Sydorenko
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
In Vivo Effects

Mesenchymal stem cells derived from bone marrow favor tumor cell growth in vivo

2006 ◽  
Vol 80 (3) ◽  
pp. 267-274 ◽  
Author(s):  
Wei Zhu ◽  
Wenrong Xu ◽  
Runqiu Jiang ◽  
Hui Qian ◽  
Miao Chen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth

Mesenchymal Stem Cells Derived from Human Adipose Tissues Favor Tumor Cell Growth in vivo

2008 ◽  
Vol 17 (3) ◽  
pp. 463-474 ◽  
Author(s):  
Ji Min Yu ◽  
Eun Sook Jun ◽  
Yong Chan Bae ◽  
Jin Sup Jung
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth ◽  
Adipose Tissues

Relationship between in vivo drug exposure of the tumor interstitium and inhibition of tumor cell growth in vitro: a study in breast cancer patients

2000 ◽  
Vol 60 (3) ◽  
pp. 211-217 ◽  
Author(s):  
Markus Müller ◽  
Julia Bockenheimer ◽  
Ulrike Zellenberg ◽  
Nikolas Klein ◽  
Günther G Steger ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Cancer Patients ◽  
Drug Exposure ◽  
Tumor Cell Growth ◽  
Breast Cancer Patients

scholarly journals miR-142-3p Suppresses Cell Growth by Targeting CDK4 in Colorectal Cancer

2018 ◽  
Vol 51 (4) ◽  
pp. 1969-1981 ◽  
Author(s):  
Xiangyu Zhu ◽  
Si-ping Ma ◽  
Dongxiang Yang ◽  
Yanlong Liu ◽  
Yong-peng Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Nude Mice ◽  
Colony Formation ◽  
Tumor Cell Growth ◽  
Rt Pcr ◽  
Tumor Tissues

Background/Aims: Deregulation of microRNAs (miRNAs) has been associated with a variety of cancers, including colorectal cancer (CRC). Here, we investigated anomalous miR-142-3p expression and its possible functional consequences in primary CRC samples. Methods: The expression of miR-142-3p was measured by quantitative RT-PCR in 116 primary CRC tissues and adjacent non-tumor tissues. The effect of miR-142-3p up- or down-regulation in CRC-derived cells was evaluated in vitro by cell viability and colony formation assays and in vivo by growth assays in xenografted nude mice. Results: Using quantitative RT-PCR, we found that miR-142-3p was down-regulated in 78.4 % (91/116) of the primary CRC tissues tested when compared to the adjacent non-tumor tissues. We also found that the miR-142-3p mimic reduced in vitro cell viability and colony formation by inducing cell cycle arrest in CRC-derived cells, and inhibited in vivo tumor cell growth in xenografted nude mice. Inversely, we found that the miR-142-3p inhibitor increased the viability and colony forming capacity of CRC-derived cells and tumor cell growth in xenografted nude mice. In addition, we identified CDK4 as a potential target of miR-142-3p by predictions and dual-luciferase reporter assays. Concordantly, we found that miR-142-3p mimics and inhibitors could decrease and increase CDK4 protein levels in CRC-derived cells, respectively. Conclusion: From our results we conclude that miR-142-3p may act as a tumor suppressor in CRC and may serve as a tool for miRNA-based CRC therapy.

GF-15, a Novel Inhibitor of Centrosomal Clustering, Suppresses Tumor Cell Growth In Vitro and In Vivo

2012 ◽  
Vol 72 (20) ◽  
pp. 5374-5385 ◽  
Author(s):  
Marc S. Raab ◽  
Iris Breitkreutz ◽  
Simon Anderhub ◽  
Mads H. Rønnest ◽  
Blanka Leber ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth

scholarly journals p120 catenin induces opposing effects on tumor cell growth depending on E-cadherin expression

2008 ◽  
Vol 183 (4) ◽  
pp. 737-749 ◽  
Author(s):  
Edwin Soto ◽  
Masahiro Yanagisawa ◽  
Laura A. Marlow ◽  
John A. Copland ◽  
Edith A. Perez ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Tumor Cell Growth ◽  
P120 Catenin ◽  
Opposing Effects ◽  
E Cadherin

p120 catenin regulates the activity of the Rho family guanosine triphosphatases (including RhoA and Rac1) in an adhesion-dependent manner. Through this action, p120 promotes a sessile cellular phenotype when associated with epithelial cadherin (E-cadherin) or a motile phenotype when associated with mesenchymal cadherins. In this study, we show that p120 also exerts significant and diametrically opposing effects on tumor cell growth depending on E-cadherin expression. Endogenous p120 acts to stabilize E-cadherin complexes and to actively promote the tumor-suppressive function of E-cadherin, potently inhibiting Ras activation. Upon E-cadherin loss during tumor progression, the negative regulation of Ras is relieved; under these conditions, endogenous p120 promotes transformed cell growth both in vitro and in vivo by activating a Rac1–mitogen-activated protein kinase signaling pathway normally activated by the adhesion of cells to the extracellular matrix. These data indicate that both E-cadherin and p120 are important regulators of tumor cell growth and imply roles for both proteins in chemoresistance and targeted therapeutics.

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