In Vitro and In Vivo Efficacy of AZD3965 and Alpha-Cyano-4-Hydroxycinnamic Acid in the Murine 4T1 Breast Tumor Model

Dendritic cells (DCs) are the most potent professional antigen-presenting cells (APCs) that mediate T-cell immune responses. Breast cancer is one of the most commonly diagnosed diseases and its mortality rate is higher than any other cancer in both humans and canines. Plantain polysaccharide (PLP), extracted from the whole plant of Plantago asiatica L., could promote the maturation of DCs. In this research, we found that PLP could upregulate the maturation of DCs both in vitro and in vivo. PLP-activated DCs could stimulate lymphocytes’ proliferation and differentiate naive T cells into cytotoxic T cells. Tumor antigen-specific lymphocyte responses were enhanced by PLP and CIPp canine breast tumor cells lysate-pulsed DCs, and PLP and CIPp-cell-lysate jointly stimulated DCs cocultured with lymphocytes having the great cytotoxicity on CIPp cells. In the 4T1 murine breast tumor model, PLP could control the size of breast tumors and improve immunity by recruiting DCs, macrophages, and CD4+ and CD8+ T cells in the tumor microenvironment. These results indicated that PLP could achieve immunotherapeutic effects and improve immunity in the breast tumor model.

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Retraction: Radio frequency triggered curcumin delivery from thermo and pH responsive nanoparticles containing gold nanoparticles and its in vivo localization studies in an orthotopic breast tumor model

RSC Advances ◽

10.1039/d0ra90082f ◽

2020 ◽

Vol 10 (48) ◽

pp. 28483-28483

Author(s):

N. Sanoj Rejinold ◽

Reju George Thomas ◽

Muthunarayanan Muthiah ◽

K. P. Chennazhi ◽

In-Kyu Park ◽

...

Keyword(s):

Gold Nanoparticles ◽

Radio Frequency ◽

Breast Tumor ◽

Tumor Model ◽

Ph Responsive ◽

Breast Tumor Model

Retraction of ‘Radio frequency triggered curcumin delivery from thermo and pH responsive nanoparticles containing gold nanoparticles and its in vivo localization studies in an orthotopic breast tumor model’ by N. Sanoj Rejinold et al., RSC Adv., 2014, 4, 39408–39427, DOI: 10.1039/C4RA05727A.

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Green Tea Polyphenol EGCG Attenuates MDSCs-mediated Immunosuppression through Canonical and Non-Canonical Pathways in a 4T1 Murine Breast Cancer Model

Nutrients ◽

10.3390/nu12041042 ◽

2020 ◽

Vol 12 (4) ◽

pp. 1042 ◽

Cited By ~ 4

Author(s):

Ping Xu ◽

Feng Yan ◽

Yueling Zhao ◽

Xiangbo Chen ◽

Shili Sun ◽

...

Keyword(s):

Breast Cancer ◽

Breast Tumor ◽

Suppressor Cells ◽

Tumor Model ◽

Receptor Interaction ◽

Green Tea Polyphenol ◽

Canonical Pathways ◽

Anti Tumor Activity

Several studies in the past decades have reported anti-tumor activity of the bioactive compounds extracted from tea leaves, with a focus on the compound epigallocatechin-3-gallate (EGCG). However, further investigations are required to unravel the underlying mechanisms behind the anti-tumor activity of EGCG. In this study, we demonstrate that EGCG significantly inhibits the growth of 4T1 breast cancer cells in vitro and in vivo. EGCG ameliorated immunosuppression by significantly decreasing the accumulation of myeloid-derived suppressor cells (MDSCs) and increasing the proportions of CD4+ and CD8+ T cells in spleen and tumor sites in 4T1 breast tumor-bearing mice. Surprisingly, a low dose of EGCG (0.5–5 μg/mL) effectively reduced the cell viability and increased the apoptosis rate of MDSCs in vitro. EGCG down-regulated the canonical pathways in MDSCs, mainly through the Arg-1/iNOS/Nox2/NF-κB/STAT3 signaling pathway. Moreover, transcriptomic analysis suggested that EGCG also affected the non-canonical pathways in MDSCs, such as ECM–receptor interaction and focal adhesion. qRT-PCR further validated that EGCG restored nine key genes in MDSCs, including Cxcl3, Vcan, Col4a1, Col8a1, Oasl2, Mmp12, Met, Itsnl and Acot1. Our results provide new insight into the mechanism of EGCG-associated key pathways/genes in MDSCs in the murine breast tumor model.

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Abstract 3267: Human population based engineered breast tumor model for in vivo biomarker discovery

10.1158/1538-7445.am10-3267 ◽

2010 ◽

Author(s):

Min Wu ◽

Kimberly Clark ◽

Nanhua Deng ◽

Zuhua Cai ◽

Megan E. Serpa ◽

...

Keyword(s):

Breast Tumor ◽

Human Population ◽

Biomarker Discovery ◽

Tumor Model ◽

Population Based ◽

Breast Tumor Model

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In Vitro and In Vivo Efficacy of the Monocarboxylate Transporter 1 Inhibitor AR-C155858 in the Murine 4T1 Breast Cancer Tumor Model

The AAPS Journal ◽

10.1208/s12248-018-0261-2 ◽

2018 ◽

Vol 21 (1) ◽

Cited By ~ 9

Author(s):

Xiaowen Guan ◽

Mark A. Bryniarski ◽

Marilyn E. Morris

Keyword(s):

Breast Cancer ◽

Tumor Model ◽

Monocarboxylate Transporter ◽

In Vivo Efficacy ◽

Monocarboxylate Transporter 1 ◽

Cancer Tumor ◽

4T1 Breast Cancer

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Estradiol Regulates Different Genes in Human Breast Tumor Xenografts Compared with the Identical Cells in Culture

Endocrinology ◽

10.1210/en.2005-0617 ◽

2006 ◽

Vol 147 (2) ◽

pp. 700-713 ◽

Cited By ~ 30

Author(s):

Djuana M. E. Harvell ◽

Jennifer K. Richer ◽

D. Craig Allred ◽

Carol A. Sartorius ◽

Kathryn B. Horwitz

Keyword(s):

Gene Expression ◽

Breast Tumor ◽

Expression Profiles ◽

Gene Expression Profiles ◽

Tumor Model ◽

Class Ii ◽

Breast Cancers ◽

Human Breast

In breast cancers, estrogen receptor (ER) levels are highly correlated with response to endocrine therapies. We sought to define mechanisms of estrogen (E) signaling in a solid breast tumor model using gene expression profiling. ER+ T47D-Y human breast cancer cells were grown as xenografts in ovariectomized nude mice under four conditions: 1) 17β-estradiol for 8 wk (E); 2) without E for 8 wk (control); 3) E for 7 wk followed by 1 wk of E withdrawal (Ewd); or 4) E for 8 wk plus tamoxifen for the last week. E-regulated genes were defined as those that differed significantly between control and E and/or between E and Ewd or control and Ewd. These protocols generated 188 in vivo E-regulated genes that showed two major patterns of regulation. Approximately 46% returned to basal states after Ewd (class I genes); 53% did not (class II genes). In addition, more than 70% of class II-regulated genes also failed to reverse in response to tamoxifen. These genes may be interesting for the study of hormone-resistance issues. A subset of in vivo E-regulated genes appears on lists of clinical ER discriminator genes. These may be useful therapeutic targets or markers of E activity. Comparison of in vivo E-regulated genes with those regulated in identical cells in vitro after 6 and 24 h of E treatment demonstrate only 11% overlap. This indicates the extent to which gene expression profiles are uniquely dependent on hormone-treatment times and the cellular microenvironment.

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Four dimensional optoacoustic imaging of perfusion in preclinical breast tumor model in vivo (Conference Presentation)

Photons Plus Ultrasound: Imaging and Sensing 2016 ◽

10.1117/12.2213112 ◽

2016 ◽

Author(s):

Xosé Luís Deán-Ben ◽

Vladimir Ermolayev ◽

Subhamoy Mandal ◽

Vasilis Ntziachristos ◽

Daniel Razansky

Keyword(s):

Breast Tumor ◽

Tumor Model ◽

Optoacoustic Imaging ◽

Breast Tumor Model

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Atovaquone Suppresses the Growth of Metastatic Triple-Negative Breast Tumors in Lungs and Brain by Inhibiting Integrin/FAK Signaling Axis

Pharmaceuticals ◽

10.3390/ph14060521 ◽

2021 ◽

Vol 14 (6) ◽

pp. 521

Author(s):

Nehal Gupta ◽

Sanjay K. Srivastava

Keyword(s):

Tumor Cells ◽

Breast Tumor ◽

Triple Negative ◽

Malignant Neoplasm ◽

Tumor Model ◽

Metastatic Tumor ◽

Mouse Heart ◽

Breast Tumor Cells

Triple-negative breast cancer (TNBC) is considered to be the most aggressive and malignant neoplasm and is highly metastatic in nature. In the current study, we investigated the anti-metastatic potential of atovaquone, a protozoal drug prescribed for Pneumocystis pneumonia. We showed that atovaquone induced apoptosis and reduced the survival of several aggressive metastatic TNBC cell lines including metastatic patient-derived cells by reducing the expression of integrin α6, integrin β4, FAK, Src, and Vimentin. In order to study the efficacy of atovaquone in suppressing metastasized breast tumor cells in brain and lungs, we performed three in vivo experiments. We demonstrated that oral administration of 50 mg/kg of atovaquone suppressed MDA-MB-231 breast tumor growth by 90% in lungs in an intravenous metastatic tumor model. Anti-metastatic effect of atovaquone was further determined by intracardiac injection of 4T1-luc breast tumor cells into the left ventricle of mouse heart. Our results showed that atovaquone treatment suppressed the growth of metastatic tumors in lungs, liver and brain by 70%, 50% and 30% respectively. In an intracranial model, the growth of HCC1806-luc brain tumors in atovaquone treated mice was about 55% less than that of control. Taken together, our results indicate the anti-metastatic effects of atovaquone in vitro and in vivo in various breast tumor metastasis models.

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