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

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 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

Role of CD10 expression in endometriosis-associated mesenchymal stem cells on the progression of endometriosis-associated carcinoma.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 5561-5561
Author(s):  
Huda Atiya ◽  
Taylor Orellana ◽  
Lan Gardner Coffman
Keyword(s):  
Ovarian Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Growth ◽  
Tumor Cell ◽  
Chemotherapy Resistance ◽  
Cd10 Expression ◽  
Sphere Formation

5561 Background: Endometriosis-associated carcinomas (EACs) such as ovarian clear cell cancer (OCCC) are rare, aggressive, chemo-resistant malignancies. While endometriosis is a known chronic inflammatory condition, the molecular mechanisms for the malignant transformation of endometriosis is unknown. Mesenchymal stem cells (MSC) are a critical component of the ovarian cancer microenvironment. Cancer cells reprogram MSCs to form carcinoma-associated MSCs (CAMSCs), which promote cancer growth, chemotherapy resistance, and metastases. MSCs are also found within the endometriotic microenvironment. CD10, a surface protein expressed by endometrial stromal cells, is also expressed on endometriosis-associated MSCs (enMSCs). Preliminary data demonstrate CD10 expression is lost in a subset of enMSCs and this loss is correlated with the acquisition of tumor-promoting properties. We hypothesized that the CD10 negative subset of enMSCs behave similarly to CAMSCs and support the growth of OCCC. Methods: EnMSCs were isolated from primary human benign endometriosis deposits involving the ovary or fallopian tubes. Flow cytometry was used to measure surface CD10 expression. We investigated the role of low CD10 enMSCs versus high CD10 enMSCs on OCCC tumor cell growth, chemotherapy resistance and stem-like cell properties in vitro and tumor cell engraftment, growth, and metastases in vivo. Luciferase-expressing OCCC cells were (1) used alone, (2) mixed with low CD10 enMSCs, or (3) mixed with high CD10 enMSCs and injected orthotopically into the ovarian bursa of NSG mice. In vivo imaging system was used to follow tumor progression and metastasis. Results: Our results demonstrated that enMSCs have variable CD10 expression. EnMSCs with low CD10 expression significantly enhanced OCCC proliferation, resistance to cisplatin, and sphere formation compared to OCCC alone. In contrast, high CD10 expressing enMSCs significantly reduce OCCC proliferation and sphere formation. Interestingly, low CD10 enMSCs selectively enhanced OCCC cell growth and had no effect on high grade serious ovarian cancer cell growth. Moreover, a reduction of CD10 expression was observed over time when high CD10 enMSCs were co-cultured with OCCC cells. Our results also showed enhanced tumor engraftment when OCCC cells were co-injected with low CD10 enMSCs to 100% one week post-injection, compared to 40% with OCCC and high CD10 enMSCs and 60% with OCCC alone. Further, mice co-injected with low CD10 enMSCs demonstrated increased metastasis and decreased survival compared to mice co-injected with high CD10 enMSCs. Conclusions: Our results indicate there is a sub population of enMSCs, marked by decreased CD10 expression, which selectively enhances OCCC growth. This highlights the existence of a tumor-promoting stromal cell within endometriosis which may be critical to the formation and propagation of EACs.

scholarly journals Opposite Effects of Coinjection and Distant Injection of Mesenchymal Stem Cells on Breast Tumor Cell Growth

2016 ◽  
Vol 5 (9) ◽  
pp. 1216-1228 ◽  
Author(s):  
Huilin Zheng ◽  
Weibin Zou ◽  
Jiaying Shen ◽  
Liang Xu ◽  
Shu Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Growth ◽  
Tumor Cell ◽  
Breast Tumor ◽  
Tumor Cell Growth ◽  
Breast Tumor Cell

scholarly journals Differential effect of subcellular localization of communication impairing gap junction protein connexin43 on tumor cell growth in vivo

Oncogene ◽  
2000 ◽  
Vol 19 (4) ◽  
pp. 505-513 ◽  
Author(s):  
V A Krutovskikh ◽  
S M Troyanovsky ◽  
C Piccoli ◽  
H Tsuda ◽  
M Asamoto ◽  
...  
Keyword(s):  
Cell Growth ◽  
Subcellular Localization ◽  
Tumor Cell ◽  
Gap Junction ◽  
Differential Effect ◽  
Tumor Cell Growth ◽  
Junction Protein ◽  
Gap Junction Protein

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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