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Py8119

Cat.No.: CSC-C6529J

Species: Mouse

Morphology: Epithelial-like

Culture Properties: Adherent

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Cat.No.
CSC-C6529J
Description
The P8119 cell line represents a mesenchymal tumor cell derived from a mammary adenocarcinoma that spontaneously arose in a MMTV-PyMY (mouse mammary tumor virus promoter driven Polyoma middle T-antigen) transgenic C57BL/6 female mouse. This cell line carries the Polyoma virus middle T oncogene, however its expression is down-regulated.
Species
Mouse
Tissue of Origin
mammary gland
Recommended Medium
F-12K Medium + 5%FBS
Culture Properties
Adherent
Morphology
Epithelial-like
Storage and Shipping
Storage condition: Liuqid Nitrogen, -180°C
Shipping: Dry Ice, Frozen
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Py8119 cells, derived from a murine breast cancer model that expresses the Polyoma Middle T (PyMT) oncogene, are a widely studied cell line known for their aggressive tumorigenic and metastatic properties. These cells exhibit hallmark features of epithelial-mesenchymal transition (EMT), including decreased E-cadherin expression and increased invasiveness, enabling them to effectively model metastatic processes like lung colonization. The PyMT-driven signaling resembles the hyperactivation of pathways including PI3K/Akt and MAPK, both of which play key roles in the progression of human breast cancer.

Currently, Py8119 cells are employed to investigate mechanisms of metastasis, interactions within the tumor microenvironment, and factors contributing to therapeutic resistance. Their robust metastatic potential makes them particularly valuable for testing anti-invasive drugs such as kinase inhibitors and EMT-targeting agents, as well as for exploring combinations of immunotherapy in syngeneic mouse models. Recent studies have also leveraged Py8119 cells to identify metastasis-suppressing genes and to dissect the effects of stromal-immune cells on tumor dissemination in co-culture systems. By bridging molecular insights with preclinical validation, Py8119 cells continue to serve as an important tool for advancing targeted therapies and deepening our understanding of aggressive breast cancer sub-types.

ΔA146Ply Inhibits TNBC Cell Migration and Invasion

The detoxified pneumolysin derivative ΔA146Ply has been proven to have a direct anti-triple negative breast cancer effect, but its work model remains unclear. In this study, The researches focused on its ability to inhibit triple-negative breast cancer metastasis.

First, scratch and transwell assays were performed to verify the effect of ΔA146Ply in MDA-MB-231, py8119, and 4T1 cells. Figure 1a-c shows that the wound was wider in the ΔA146Ply group than in the medium group. Furthermore, the number of migrating and invading cells was significantly lower in the ΔA146Ply group than that in the medium group (Fig. 1d-i). These results indicate that ΔA146Ply suppressed TNBC cell migration and invasion.

After ΔA146Ply treatment, TNBC cells migrating and invading through transwell inserts towards serum are shown.Fig. 1. ΔA146Ply inhibits TNBC cell migration and invasion (Zhang, Hong, et al. 2024).

ARIH1 Regulates MAP4, a Microtubule-Associated Protein, in Breast Cancer Cells

Chemotherapy drugs like paclitaxel are widely used to treat breast cancer by stabilizing microtubules, structures essential for cell division. However, resistance to paclitaxel limits its effectiveness in many patients. In this study, the researchers identify ARIH1, a protein that regulates microtubule stability, as a potential therapeutic target and biomarker in breast cancer.

The researchers stably silenced ARIH1 in both SUM159 and Py8119 cells through shRNA KD and CRISPR Cas9 KO, respectively (Fig. 2A). MAP4 is a microtubule-associated protein known to regulate microtubule stability. Western blot analysis confirmed the differential expression of MAP4 in PY8119 and SUM159 cells under various conditions (Fig. 2B, C). These results suggest that ARIH1 negatively regulates MAP4 protein levels, either directly or indirectly. Immunofluorescence analysis revealed a spatial relationship between MAP4 and beta-tubulin in PY8119 and SUM159 cells (Fig. 2D). This was accompanied by the formation of prominent microtubule bundles. These findings suggest that ARIH1 deficiency leads to increased MAP4 expression and localization to microtubules.

Western blot and Immunofluorescence analysis of MAP4 expression in PY8119 and Sum159 cells.Fig. 2. ARIH1 regulates MAP4 to modulate microtubule stability (Elshaer, Mohamed, Breege V. Howley, and Philip H. Howe. 2025).

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