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首页> 外文期刊>Clinical and experimental metastasis >Dormancy and growth of metastatic breast cancer cells in a bone-like microenvironment
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Dormancy and growth of metastatic breast cancer cells in a bone-like microenvironment

机译：骨样微环境中转移性乳腺癌细胞的休眠和生长

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Breast cancer can reoccur, often as bone metastasis, many years if not decades after the primary tumor has been treated. The factors that stimulate dormant metastases to grow are not known, but bone metastases are often associated with skeletal trauma. We used a dormancy model of MDA-MB-231BRMS1, a metastasis-suppressed human breast cancer cell line, co-cultured with MC3T3-E1 osteoblasts in a long term, three dimensional culture system to test the hypothesis that bone remodeling cytokines could stimulate dormant cells to grow. The cancer cells attached to the matrix produced by MC3T3-E1 osteoblasts but grew slowly or not at all until the addition of bone remodeling cytokines, TNF alpha and IL-beta. Stimulation of cell proliferation by these cytokines was suppressed with indomethacin, an inhibitor of cyclooxygenase and of prostaglandin production, or a prostaglandin E2 (PGE2) receptor antagonist. Addition of PGE2 directly to the cultures also stimulated cell proliferation. MCF-7, non-metastatic breast cancer cells, remained dormant when co-cultured with normal human osteoblast and fibroblast growth factor. Similar to the MDA-MB-231BRMS1 cells, MCF-7 proliferation increased in response to TNF alpha and IL-beta. These findings suggest that changes in the bone microenvironment due to inflammatory cytokines associated with bone repair or excess turnover may trigger the occurrence of latent bone metastasis.
机译：乳腺癌可以在原发性肿瘤治疗后很多年（即使不是几十年）复发，通常是骨转移。刺激休眠转移生长的因素尚不清楚，但骨转移通常与骨骼创伤有关。我们使用MDA-MB-231BRMS1（一种转移抑制的人乳腺癌细胞系）的休眠模型，将其与MC3T3-E1成骨细胞长期，三维培养系统共培养，以检验骨骼重塑细胞因子可以刺激休眠的假说细胞生长。癌细胞附着在MC3T3-E1成骨细胞产生的基质上，但生长缓慢或根本不生长，直到添加了骨重塑细胞因子，TNFα和IL-β。消炎痛抑制了这些细胞因子对细胞增殖的刺激，消炎痛是一种环氧合酶和前列腺素产生的抑制剂，或者是一种前列腺素E2（PGE2）受体拮抗剂。将PGE 2直接添加到培养物中也刺激细胞增殖。与正常人成骨细胞和成纤维细胞生长因子共同培养时，MCF-7（非转移性乳腺癌细胞）保持休眠状态。与MDA-MB-231BRMS1细胞相似，MCF-7增殖响应TNFα和IL-β而增加。这些发现表明，由于与骨修复相关的炎性细胞因子引起的骨微环境变化或过度的周转可能触发潜在的骨转移。

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