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Stromal ERalpha Normalized Angiogenesis in ER-Negative Tumor


, : Stromal ERalpha Normalized Angiogenesis in ER-Negative Tumor.

Estrogens directly promote the growth of breast cancers that express the estrogen receptor ? (ER?). However, the contribution of stromal expression of ER? in the tumor microenvironment to the protumoral effects of estrogen has never been explored. In this study, we evaluated the molecular and cellular mechanisms by which 17?-estradiol (E2) impacts the microenvironment and modulates tumor development of ER?-negative tumors. Using different mouse models of ER-negative cancer cells grafted subcutaneously into syngeneic ovariectomized immunocompetent mice, we found that E2 potentiates tumor growth, increases intratumoral vessel density, and modifies tumor vasculature into a more regularly organized structure, thereby improving vessel stabilization to prevent tumor hypoxia and necrosis. These E2-induced effects were completely abrogated in ER?-deficient mice, showing a critical role of host ER?. Notably, E2 did not accelerate tumor growth when ER? was deficient in Tie2-positive cells, even in mice grafted with wild-type bone marrow. These results were extended by clinical evidence of ER?-positive stromal cell labeling in the microenvironment of human breast cancers. Together, our findings therefore show that E2 promotes the growth of ER?-negative cancer cells through the activation of stromal ER? (extra-hematopoietic Tie-2 positive cells), which normalizes tumor angiogenesis and allows an adaptation of blood supply to tumors, thereby preventing hypoxia and necrosis. These findings significantly deepen mechanistic insights into the impact of E2 on tumor development with potential consequences for cancer treatment.

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