Growth Inhibition of Breast Tumor Cells by Hypodense and Normodense Eosinophilic Cell Lines

1999 ◽  
Author(s):  
Paulette M. Furbert-Harris
Keyword(s):  
Growth Inhibition ◽  
Tumor Cells ◽  
Cell Lines ◽  
Breast Tumor ◽  
Breast Tumor Cells ◽  
Eosinophilic Cell

scholarly journals Productive Infection of Human Breast Cancer Cell Lines with Human Cytomegalovirus (HCMV)

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 641
Author(s):  
Kaitlin M. Branch ◽  
Erica C. Garcia ◽  
Yin Maggie Chen ◽  
Matthew McGregor ◽  
Mikayla Min ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Breast Tumor Cells

Breast cancer is the leading cause of cancer deaths among women worldwide. There are many known risk factors for breast cancer, but the role of infectious disease remains unclear. Human cytomegalovirus (HCMV) is a widespread herpesvirus that usually causes little disease. Because HCMV has been detected in breast tumor biopsy samples and is frequently transmitted via human breast milk, we investigated HCMV replication in breast tumor cells. Four human breast cancer cell lines with different expression profiles for the key diagnostic markers of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), were infected with a bacterial artificial chromosome-derived HCMV clinical strain TB40/E tagged with green fluorescent protein (GFP). Fluorescence microscopy confirmed that all four breast cancer cell lines supported virus entry. RNA was isolated from infected cells and the expression of immediate early (UL123), early (UL54), and late (UL111A) genes was confirmed using PCR. Viral proteins were detected by immunoblotting, and viral progeny were produced during the infection of breast tumor cells, as evidenced by subsequent infection of fibroblasts with culture supernatants. These results demonstrate that breast tumor cells support productive HCMV infection and could indicate that HCMV replication may play a role in breast cancer progression.

The role of TGF-β production in growth inhibition of breast-tumor cells by progestins

1995 ◽  
Vol 61 (1) ◽  
pp. 80-86 ◽  
Author(s):  
Eric Kalkhoven ◽  
Linda Kwakkenbos-Isbrücker ◽  
Christine L. Mummery ◽  
Siegfried W. De Laat ◽  
Adriana J. M. Van Den Eijnden-Van Raaij ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Breast Tumor Cells

Growth inhibition by anti-estrogens and progestins in TGF-β-resistant and -sensitive breast-tumor cells

1996 ◽  
Vol 65 (5) ◽  
pp. 682-687 ◽  
Author(s):  
Eric Kalkhoven ◽  
Eliana Beraldi ◽  
M. Luisa Panno ◽  
Johan P. De Winter ◽  
Jos H. H. Thijssen ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Breast Tumor Cells

scholarly journals Platelets Promote Breast Cancer Metastasis By Reprogramming Tumor Cells to Produce IL-8

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2233-2233
Author(s):  
Kelly Elizabeth Johnson ◽  
Kellie R Machlus ◽  
Saleh El-Husayni ◽  
Rajesh Kulenthirarajan ◽  
Jodi A Forward ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Lines ◽  
Breast Tumor ◽  
Receptor Expression ◽  
Breast Tumor Cells ◽  
Egfr Inhibition ◽  
Platelet Releasate ◽  
Mcf 7

Abstract Platelets, primarily known for their role in hemostasis, are now recognized to play an integral role in cancer progression and metastasis. Recent evidence has established that platelets are activated by contact with breast tumor cells, leading to the release of hundreds of growth factors, cytokines, chemokines and angiogenesis mediators that could influence tumor growth and metastasis. Indeed, work from our group has demonstrated that factors released from activated platelets promote both metastasis and angiogenesis. However, little is known about the specific factors and signaling pathways that mediate this critical platelet-tumor cell cross-talk. To address this question, we performed an angiogenesis array (Ray Biotech) to identify specific pro-angiogenic and pro-metastatic factors released by tumor cells during platelet-tumor cell interactions. We identified several factors that were secreted by MCF-7 breast tumor cells in response to activated platelet releasate, including high levels of interleukin 8 (IL-8, CXCL8). IL-8 is a cytokine known to play a critical role in metastasis and angiogenesis and is elevated in the serum and tumor tissue of breast cancer patients. We confirmed that exposure to platelets strongly induced the production of IL-8 in several human breast cancer cell lines (MDA-MB-231, BT-20, SKBR-3 and MCF-7) by ELISA and found that platelets themselves do not contain detectable levels of IL-8. Furthermore, IL-8 production was highest in the more aggressive, triple negative MDA-MB-231 and BT-20 lines, suggesting a link between platelet-induced IL-8 and tumor subtype. To identify the specific component or components of platelet releasate responsible for driving tumor cell IL-8, we first characterized the contents of activated platelet releasate by array (Ray Biotech) and found an abundance of both chemokine (C-C motif) ligand 5 (CCL5, RANTES) and epidermal growth factor (EGF). Next, we treated breast tumor cell lines directly with recombinant CCL5 or EGF and observed an increase in IL-8 production, however sensitivity to CCL5, EGF or the combination varied among the cell lines tested and may depend on receptor expression. To determine if platelet-derived CCL5 or EGF drives tumor cell IL-8, breast tumor cells were pretreated with the CCL5 receptor (CCR5) blocker maraviroc or the EGFR blocker AG-1478 and then exposed to platelets. Blocking CCR5 abrogated the induction of IL-8 in response to platelets in the cell lines that were sensitive to CCL5 while EGFR inhibition diminished induction of IL-8 in response to platelets in the cell lines that were sensitive to EGF. Next we sought to determine the role of platelet-induced IL-8 in metastasis. We performed standard invasion assays using MDA-MB-231 cells transfected with IL-8shRNA or control cells. Platelets were able to increase the invasion of control MDA-MD-231 cells by 5 fold, while IL-8 knockdown reduced the effect of platelets on invasion by 50%. Furthermore, ability of platelets to promote tumor cell migration across an endothelialized membrane was reduced 87% in IL-8 knockdown MDA-MB-231s compared to controls in standard transendothelial migration assays. These results suggest that platelets promote metastasis, in part, by driving tumor cell IL-8. Studies are currently underway to further elucidate the mechanism by which platelets reprogram tumor cells to produce IL-8 and to confirm these findings in vivo. Taken together, these results suggest that platelets, through release of soluble factors, drive tumor cells to produce IL-8 and that blocking this communication can disrupt the pro-metastatic potential of platelets. Ultimately, these studies support targeting specific platelet-tumor cell interaction as a novel means of limiting disease progression in breast cancer. Disclosures No relevant conflicts of interest to declare.

scholarly journals Antiproliferative Effect of Electric Fields on Breast Tumor Cells In Vitro and In Vivo

2017 ◽  
Vol 6 (3) ◽  
pp. 71 ◽  
Author(s):  
Firman Alamsyah ◽  
Izzatun Niswah Ajrina ◽  
Fitriya Nur Annisa Dewi ◽  
Diah Iskandriati ◽  
Silvia Arin Prabandari ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Breast Tissue ◽  
In Vitro Study ◽  
Mammary Glands ◽  
Breast Tumor Cells ◽  
Mcf 7

Our research focused on the antiproliferative effect of low intensity (18 Vpp) and intermediate frequency (100 KHz) electrostatic wave between two capacitive electrodes on breast tumor cells in vitro and in vivo. In vitro study has been conducted by using MCF-7 cell lines treated with external electrostatic for 24, 48, and 72 hours of treatment and the cells number were calculated during treatment by using hemocytometer and presented as Growth Inhibition (GI)% efficacy. For in vivo, we used female mice (Mus musculus) strain C3H as animal model. The mice were injected with either MCF-7 cells, mammary tumor cells from C3H donor, or NaCl 0.9% (placebo) subcutaneously into the axilla area and exposed by external electrostatic in each cage for 12 hours in 2 weeks before necropsied. The adjacent and breast tissue were collected and stained with Hematoxylin – Eosin then analyzed for histopathological profile. In vitro study revealed the number of exposed cells decreased with lower proliferation rate than the non-exposed cells. Moreover, the external electrostatic caused 28-39% growth inhibition efficacy of MCF-7 cells. After 2 weeks of exposure, placebo mice were physically normal, whereas the tumor undergone significant shrinkage of more than 67% in size. Histopathological analysis of the mammary glands indicated infiltration of macrophages into the tumor area through the blood vessel. No abnormality was found in the skin layer and mammary glands of the breast tissue of placebo mice. Here, we present new knowledge of electro-capacitive cancer therapy (ECCT) as a novel treatment modality.Keywords : ECCT, tumor, in vitro, in vivo, breast cancer cells, antiproliferative

Suspension state promotes extravasation of breast tumor cells by increasing integrin β1 expression

BIOCELL ◽  
2018 ◽  
Vol 42 (1) ◽  
pp. 17-24 ◽  
Author(s):  
B. Zhang ◽  
Y. Zhang ◽  
X. Zhang ◽  
Y. LV
Keyword(s):  
Tumor Cells ◽  
Breast Tumor ◽  
Integrin Β1 ◽  
Breast Tumor Cells
Sign in / Sign up

Export Citation Format

Share Document