Comparative Profiling of Metastatic 4T1- vs. Non-metastatic Py230-Based Mammary Tumors in an Intraductal Model for Triple-Negative Breast Cancer

Steenbrugge, Jonas; Elst, Niels Vander; Demeyere, Kristel; Wever, Olivier De; Sanders, Niek N.; Broeck, Wim Van Den; Dirix, Luc; Laere, Steven Van; Meyer, Evelyne

doi:10.3389/fimmu.2019.02928

Cited by 33 publications

(43 citation statements)

References 90 publications

(104 reference statements)

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“…Following intraductal inoculation of luciferase-expressing 4T1 tumor cells through the teat canal of syngeneic and lactating BALB/c mice, primary tumors were allowed to grow for 21 days. Based on previous studies by our group [15][16][17][18] and cytokeratin 5 stainings for myoepithelial cells, 4T1 tumor cells remained inside the mammary ducts surrounded by an intact epithelial barrier until 7 days post inoculation (p.i. ), characteristic for the ductal carcinoma in situ (DCIS) stage (Fig.…”

Section: Omo-1 Decreases Non-c-met Addicted Tumor Progression and Hasmentioning

confidence: 94%

“…OMO-1 decreases neutrophil infiltration, induces immune stimulation, and in combination with cisplatin reduces tumorassociated macrophages (TAMs) Splenomegaly has been associated with 4T1 tumor progression and leukemoid reactions 15,16,[18][19][20][21] . Based on spleen weights, tumor-bearing mice receiving vehicle suffered from severe splenomegaly ( Supplementary Fig.…”

Section: Omo-1 Decreases Non-c-met Addicted Tumor Progression and Hasmentioning

confidence: 99%

“…Here, we evaluated the efficacy of OMO-1 in an innovative 4T1based immunocompetent intraductal mouse model for TNBC. In contrast to the classical fat pad model, the intraductal model more closely resembles the human disease process as intraductally inoculated tumors grow from within the mammary ducts and undergo ductal breakthrough to invade the mammary fat pad and metastasize to distant organs [15][16][17][18] . The use of immunocompetent mice allows to study the possible impact of OMO-1 on tumor immunology.…”

Section: Introductionmentioning

confidence: 99%

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OMO-1 reduces progression and enhances cisplatin efficacy in a 4T1-based non-c-MET addicted intraductal mouse model for triple-negative breast cancer

et al. 2021

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Abstractc-MET is considered a driver of cancer progression, impacting tumor growth and tumor-supporting stroma. Here, we investigated the therapeutic efficacy of OMO-1, a potent and selective c-MET inhibitor, in an immunocompetent intraductal mouse model for triple-negative breast cancer (TNBC). OMO-1 reduced non-c-MET addicted 4T1 tumor progression dose dependently as monotherapeutic and provided additional disease reduction in combination with cisplatin. At the stromal level, OMO-1 significantly reduced neutrophil infiltration in 4T1 tumors, promoted immune activation, and enhanced cisplatin-mediated reduction of tumor-associated macrophages. OMO-1 treatment also reduced 4T1 tumor hypoxia and increased expression of pericyte markers, indicative for vascular maturation. Corroborating this finding, cisplatin delivery to the 4T1 primary tumor was enhanced upon OMO-1 treatment, increasing cisplatin DNA-adduct levels and tumor cell death. Although verification in additional cell lines is warranted, our findings provide initial evidence that TNBC patients may benefit from OMO-1 treatment, even in cases of non-c-MET addicted tumors.

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Section: Omo-1 Decreases Non-c-met Addicted Tumor Progression and Hasmentioning

confidence: 94%

Section: Omo-1 Decreases Non-c-met Addicted Tumor Progression and Hasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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OMO-1 reduces progression and enhances cisplatin efficacy in a 4T1-based non-c-MET addicted intraductal mouse model for triple-negative breast cancer

et al. 2021

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“…Considering that the growth of tumours can be observed directly in animal experiments in vivo and that tumour tissues can be assessed more conveniently, we used the mouse 4T1 breast cancer animal model to study the inhibitory effect of SGHZF on TNBC. This model is a recognized animal model of TNBC in mice, and its tumour growth rate and metastasis status are very similar to those of humans, which makes it an ideal animal model for the study of TNBC [ 25 , 26 ]. In this study, we calculated the tumour volume of mice in this model and found that the tumour volume and tumour inhibition rate of different experimental groups did not change over time.…”

Section: Discussionmentioning

confidence: 99%

The Shuganhuazheng Formula in Triple‐Negative Breast Cancer: A Study Based on Network Pharmacology and In Vivo Experiments

Wang

Fei

Yang

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Breast cancer is the most common cancer in women. Among breast cancer subtypes, triple-negative breast cancer (TNBC) has the highest degree of malignancy and the worst prognosis. The Shuganhuazheng formula (SGHZF) is a traditional Chinese herbal formula for the treatment of TNBC, but the mechanism of SGHZF in the treatment of TNBC remains unclear. In this study, the therapeutic effect and mechanism of SGHZF against TNBC were preliminarily determined based on in vivo experimental verification and network pharmacology. In terms of therapeutic effects, the antitumour effect was verified by measuring and calculating tumour volume, and the expression of proto-oncogene c-Myc was verified by PCR. In terms of the mechanism, potential therapeutic targets were identified by overlapping the SGHZF-related and TNBC-related targets. After comprehensively analysing the results of the protein-protein interaction (PPI), gene ontology (GO) function, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, Akt and HIF-1α were selected for verification by using immunohistochemical and Western blot analyses. The results of the study indicated that SGHZF can inhibit breast tumour growth in mice and that the mechanism may be related to the inhibition of Akt and HIF-1α expression.

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“…Radiation would seem to create a fertile niche for CTCs and metastases. In BALB/c mice, the in-breast injection of a mammary carcinoma tumor cell line (4T1) after 9 Gy of half chest photon irradiation led to a higher incidence of lung metastasis and shorter survival [ 73 , 74 ]. Still, 2 Gy of abdomen irradiation, before colon cancer cells intravenous injection, increased the mice mortality due to higher lung metastasis.…”

Section: Circulating Tumor Cells and Radiationmentioning

confidence: 99%

Tumor Hypoxia and Circulating Tumor Cells

Tinganelli

Durante

2020

IJMS

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Circulating tumor cells (CTCs) are a rare tumor cell subpopulation induced and selected by the tumor microenvironment’s extreme conditions. Under hypoxia and starvation, these aggressive and invasive cells are able to invade the lymphatic and circulatory systems. Escaping from the primary tumor, CTCs enter into the bloodstream to form metastatic deposits or re-establish themselves in cancer’s primary site. Although radiotherapy is widely used to cure solid malignancies, it can promote metastasis. Radiation can disrupt the primary tumor vasculature, increasing the dissemination of CTCs. Radiation also induces epithelial–mesenchymal transition (EMT) and eliminates suppressive signaling, causing the proliferation of existent, but previously dormant, disseminated tumor cells (DTCs). In this review, we collect the results and evidence underlying the molecular mechanisms of CTCs and DTCs and the effects of radiation and hypoxia in developing these cells.

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Comparative Profiling of Metastatic 4T1- vs. Non-metastatic Py230-Based Mammary Tumors in an Intraductal Model for Triple-Negative Breast Cancer

Cited by 33 publications

References 90 publications

OMO-1 reduces progression and enhances cisplatin efficacy in a 4T1-based non-c-MET addicted intraductal mouse model for triple-negative breast cancer

OMO-1 reduces progression and enhances cisplatin efficacy in a 4T1-based non-c-MET addicted intraductal mouse model for triple-negative breast cancer

The Shuganhuazheng Formula in Triple‐Negative Breast Cancer: A Study Based on Network Pharmacology and In Vivo Experiments

Tumor Hypoxia and Circulating Tumor Cells

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