Differential effects of p95HER2 and FL-HER2 on gene expression in PB2 mouse breast tumor xenografts at early and late stages.
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PROVIDER: PRJNA1078310 | ENA |
REPOSITORIES: ENA
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Project description:To explore how p95HER2 regulates gene expression to promote tumor growth in immunocompetent mice, we engineered PB2 mouse breast cancer cells to express either p95HER2 or control FL-HER2 under the control of doxycycline. Both FL-HER2 and p95HER2 cells were implanted to the mammary fat pads of immunocompetent C57BL/6 mice that were placed under a DOX625 doxycycline diet. Tumor xenografts were harvested 10 and 22 days after inoculation. We then performed transcriptomic analysis using RNA-seq data from PB2-FL-HER2 and PB2-p95HER2 tumors.
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Project description:To explore how p95HER2 regulates gene expression to promote tumor growth in immunocompetent mice, we engineered PB2 mouse breast cancer cells to express p95HER2 under the control of doxycycline. Both empty vector (EV) and p95HER2 cells were implanted to the mammary fat pads of immunocompetent C57BL/6 mice, which were placed under a DOX625 doxycycline diet. Tumor xenografts were harvested 3 weeks after inoculation. We then performed transcriptomic analysis using the RNA-seq data from PB2-EV and PB2-p95HER2 tumors.
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Project description:Breast cancer research is hampered by difficulties in obtaining and studying primary human breast tissue, and by the lack of in vivo preclinical models that reflect patient tumor biology accurately. To overcome these limitations, we propagated a cohort of human breast tumors grown in the epithelium-free mammary fat pad of SCID/Beige and NOD/SCID/IL2γ-receptor null (NSG) mice, under a series of transplant conditions. Both models yielded stably transplantable xenografts at comparably high rates (~23% and ~19%, respectively). Of the conditions tested, xenograft take rate was highest in the presence of a low-dose estradiol pellet. Overall, 32 stably transplantable xenograft lines were established, representing unique 25 patients. Most tumors yielding xenografts were “triple-negative” (ER-PR-HER2+) (n=19). However, we established lines from three ER-PR-HER2+ tumors, one ER+PR-HER2-, one ER+PR+HER2- and one “triple-positive” (ER+PR+HER2+) tumor. Serially passaged xenografts show biological consistency with the tumor of origin, are phenotypic stability across multiple transplant generations at the histological, transcriptomic, proteomic, and genomic levels, and show comparable treatment responses. Xenografts representing 12 patients, including two ER+ lines, showed metastasis to the mouse lung. These models thus serve as a renewable, quality-controlled tissue resource for preclinical studies investigating treatment response and metastasis.
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