scholarly journals Selective antitumor effect of neural stem cells expressing cytosine deaminase and interferon-beta against ductal breast cancer cells in cellular and xenograft models

2014 ◽  
Vol 12 (1) ◽  
pp. 36-48 ◽  
Author(s):  
Bo-Rim Yi ◽  
Kyung-A. Hwang ◽  
Karen S. Aboody ◽  
Eui-Bae Jeung ◽  
Seung U. Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Antitumor Effect ◽  
Interferon Beta ◽  
Cytosine Deaminase ◽  
Ductal Breast Cancer ◽  
Xenograft Models

207 ENGINEERED HUMAN AMNIOTIC FLUID-DERIVED STEM CELLS BY EXPRESSING CYTOSINE DEAMINASE (CD) AND THYMIDINE KINASE (HSV-TK) MEDIATE TARGETING KILLING EFFECT IN BREAST CANCER CELLS

2012 ◽  
Vol 24 (1) ◽  
pp. 216 ◽  
Author(s):  
N.-H. Kang ◽  
K.-C. Choi
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Amniotic Fluid ◽  
Cancer Cells ◽  
Thymidine Kinase ◽  
Breast Cancer Cells ◽  
Active Form ◽  
Cytosine Deaminase ◽  
Human Amniotic Fluid ◽  
Suicide Genes

Genetically engineered stem cells (GESTECs) expressing suicide genes which can convert non-toxic prodrugs to toxic metabolites have been shown to reduce tumour growth. In this sudy, we employed human amniotic fluid-derived stem cells (hAFSCs) as a source of cells for suicide gene transfer. hAFSCs were engineered to express multiple suicide genes, a bacterial cytosine deaminase (CD) and herpes simplex virus thymidine kinase (HSV-TK) genes. Thus, AF2.CD-TK cells were generated to express CD and HSV-TK genes simultaneously, which can convert 5-fluorocytosine (5-FC) and monophosphorylate ganciclovir (GCV-MP) into 5-fluorouracil (5-FU) and active form of triphosphate ganciclovir (GCV-TP), respectively. Combination of CD and HSV-TK suicide genes in AF2.CD-TK cells resulted in enhanced antitumour activity in vitro and in vivo xenograft models. AF2.CD-TK cells significantly inhibited the growth of MDA-MB-231 human breast cancer cells in the presence of the prodrugs, 5-FC and GCV, by MTT assay. MDA-MB-231 cells were implanted into the right mammary fat pad of female BALB/c nude mice and CM-DiI-labelled AF2.CD-TK cells were injected into the circumtumoral site with 5-FC (500 mg kg–1 day–1) and GCV (10 mg kg–1 day–1). Treatment of the mice with AF2.CD-TK cells significantly reduced tumour volumes in MDA-MB-231 xenografted mice. We further evaluated tumour progression by histopathological and fluorescent staining. Taken together, these results indicate that AF2.CD-TK cells can serve as a vehicle for a novel therapeutic approach enzyme/prodrug system to selectively target breast malignancies. This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2011-0015385).

scholarly journals Biomechanical regulation of breast cancer metastasis and progression

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Adrianne Spencer ◽  
Andrew D. Sligar ◽  
Daniel Chavarria ◽  
Jason Lee ◽  
Darshil Choksi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Mechanical Load ◽  
Breast Cancer Metastasis ◽  
Proliferation And Metastasis ◽  
Xenograft Models ◽  
Chemotherapeutic Treatment ◽  
Complex Signaling

AbstractPhysical activity has been consistently linked to decreased incidence of breast cancer and a substantial increase in the length of survival of patients with breast cancer. However, the understanding of how applied physical forces directly regulate breast cancer remains limited. We investigated the role of mechanical forces in altering the chemoresistance, proliferation and metastasis of breast cancer cells. We found that applied mechanical tension can dramatically alter gene expression in breast cancer cells, leading to decreased proliferation, increased resistance to chemotherapeutic treatment and enhanced adhesion to inflamed endothelial cells and collagen I under fluidic shear stress. A mechanistic analysis of the pathways involved in these effects supported a complex signaling network that included Abl1, Lck, Jak2 and PI3K to regulate pro-survival signaling and enhancement of adhesion under flow. Studies using mouse xenograft models demonstrated reduced proliferation of breast cancer cells with orthotopic implantation and increased metastasis to the skull when the cancer cells were treated with mechanical load. Using high throughput mechanobiological screens we identified pathways that could be targeted to reduce the effects of load on metastasis and found that the effects of mechanical load on bone colonization could be reduced through treatment with a PI3Kγ inhibitor.

Exosomal MicroRNA-204 Derived from Bone Marrow Mesenchymal Stem Cells (BMSCs) Inhibits Cell Proliferation and Induces Apoptosis Through NF-κB Signaling Pathway in Breast Cancer

2022 ◽  
Vol 12 (2) ◽  
pp. 273-278
Author(s):  
Daqing Jiang ◽  
Xianxin Xie ◽  
Cong Wang ◽  
Weijie Li ◽  
Jianjun He
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Marrow Mesenchymal Stem Cells ◽  
Induced Apoptosis ◽  
Signaling Activation

Our study intends to assess the relationship between exosomes derived from bone marrow mesenchymal stem cells (BMSC-exo) and breast cancer. BMSC-exo were isolated and characterized by transmission electron microscopy. After transfection of BMSCs with miR-204 inhibitor, breast cancer cells were incubated with BMSC-exo followed by analysis of cell proliferation by CCK-8 assay, cell apoptosis by flow cytometry, and expression of apoptosis-related protein and NF-κB signaling by western blot. The co-culture of BMSC-exo with breast cancer cells enhanced miR-204 transcription, inhibited cell proliferation and induced apoptosis. Further, BMSC-exo accelerated apoptosis as demonstrated by the increased level of Bax and casepase-3 and decreased Bcl-2 expression, as well as reduced NF-κB signaling activity. But knockdown of miR-204 abolished the effect of BMSC-exo on apoptosis and proliferation with NF-κB signaling activation. In conclusion, miR-204 from BMSC-exo restrains growth of breast cancer cell and might be a novel target for treating breast cancer.

Application of digital holographic tumography in antitumor effect of cantharides complex on 4T1 breast cancer cells

2021 ◽  
Vol 60 (12) ◽  
pp. 3365
Author(s):  
Chen-Wen Lu ◽  
Andrey V. Belashov ◽  
Anna A. Zhikhoreva ◽  
Irina V. Semenova ◽  
Chau-Jern Cheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Antitumor Effect ◽  
4T1 Breast Cancer

scholarly journals Dysregulation of Transcription Factor EB Contributes to Cell Proliferation, Metastasis and Stemness in Breast Cancer

2021 ◽  
Author(s):  
Ningwei Fu ◽  
Ning Fan ◽  
Wenchao Luo ◽  
Lijia Lv ◽  
Jing Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Breast Cancer Stem Cells ◽  
Cancer Proliferation ◽  
Mammosphere Formation

Abstract Purpose: TFEB is a key regulator of autophagy-lysosomal biogenesis pathways, while its dysregulation is highly prevalent in various human cancers, but the specific contribution to breast cancer remains poorly understood. The main purpose of this study is to explore the role of TFEB in breast cancer proliferation, metastasis and maintaining breast cancer stem cells (BCSCs) traits, thus uncovering its underlying mechanism.Methods: Bioinformatics, western blotting and immunohistochemical staining were applied to analyze the expression of TFEB in breast cancer. Stable down-regulation TFEB cells were established in MCF-7 and MDA-MB-231 breast cancer cell lines. MTT, clone formation, wound healing, transwell and 3D tumor invasion assays were used to evaluate the proliferation, migration and invasion ability of breast cancer cells. Mammosphere formation, immunocytochemical (ICC) staining were used to detect the effect of down-regulating TFEB on breast cancer stem cells. Results: we demonstrated that higher expression of TFEB was found in breast cancer. TFEB depletion had inhibitory effects on cellular proliferation, migration and invasion of breast cancer cells. Moreover, knockdown TFEB decreased mammosphere formation ability of BCSCs and expression of cancer stem cell markers. Autophagy-lysosomal related proteins were decreased by down regulation of TFEB. Conclusion: we uncovered a critical role of TFEB in breast cancer proliferation and metastasis, and BCSCs self-renewal and stemness. The underlying mechanisms involve in maintaining BCSCs traits, and dysregulating lysosome functions.

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