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RNA-seq data for studying the influence of fallopian tube stromal cells and/or estrogen treatment on fallopian tube epithilial cells

ABSTRACT: This study aims to investigate the role of fallopian tube (FT) stromal cells (SCs) in supporting the growth, proliferation and differentiation of fallopian tube epithelial (FTE) cells in response to estrogen signaling. Estrogen receptor alpha (encoded by Esr1) positive cells are present in both FTE and FT stromal compartments. Thus, estrogen exposure can affect FTE cells either directly or indirectly via Esr1+ SCs. Here we used RNA-seq expression profiling of murine FTE cells under various treatment conditions to demonstrate how estradiol (E2) treatment affected their transcriptomics directly, and indirectly via the co-cultured FT SCs, utilizing an organoid culture/co-culture system.

ORGANISM(S): Mus musculus

PROVIDER: GSE310469 | GEO | 2026/01/21

REPOSITORIES: GEO

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Project description:Recent evidence suggests that ovarian high-grade serous carcinoma (HGSC) originates from the epithelium of the fallopian tube. However, most mouse models are based on the previous prevailing view that ovarian cancer develops from the transformation of the ovarian surface epithelium. Here, we report the extensive histological and molecular characterization of the mogp-TAg transgenic mouse, which expresses the SV40 large T-antigen (TAg) under the control of the mouse müllerian-specific Ovgp-1 promoter. Histologic analysis of the fallopian tubes of mogp-TAg mice identified a variety of neoplastic lesions analogous to those described as precursors to ovarian HGSC. We identified areas of normal appearing p53-positive epithelium that are similar to “p53 signatures” in the human fallopian tube. More advanced proliferative lesions with nuclear atypia and epithelial stratification were also identified that were morphologically and immunohistochemically reminiscent of human serous tubal intraepithelial carcinoma (STIC), a potential precursor of ovarian HGSC. Beside these noninvasive precursor lesions, we also identified invasive adenocarcinoma in the ovary of 56% of the mice. Microarray analysis revealed several genes differentially expressed between the fallopian tube of mogp-TAg and WT C57BL/6. One of these genes, Top2a, which encodes topoisomerase II-alpha, was shown by immunohistochemistry to be concurrently expressed with elevated p53 and specifically elevated in mouse STICs, but not in surrounding tissues. TOP2A protein was also found elevated in human STICs, low-grade, and high-grade serous carcinoma. The mouse model reported here displays a progression from normal tubal epithelium to invasive HGSC in the ovary, and therefore closely simulates the current emerging model of human ovarian HGSC pathogenesis. This mouse therefore has the potential to be a very useful new model for elucidating the mechanisms of serous ovarian tumorigenesis, as well as for developing novel approaches for the prevention, diagnosis, and therapy of this disease. Keywords: transgenic mouse model, ovarian cancer, fallopian tube, intraepithelial carcinoma 6 mouse fallopian tubes (FT) were analyzed with experimental repeats; 3 wildtype C57BL6 mice (FT) and 3 transgenic mogp-TAg (FT), with one set of each at 7, 8 and 9 weeks of age.

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RNA-seq data for studying the influence of fallopian tube stromal cells and/or estrogen treatment on fallopian tube epithilial cells

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