Pineda M J, Lu Z, Cao D, Kim J J
Division of Gynecologic Oncology, Northwestern University, Chicago, IL, USA.
Horm Cancer. 2015 Aug;6(4):131-41. doi: 10.1007/s12672-015-0223-4. Epub 2015 May 15.
Cancer-associated fibroblasts have been shown to inhibit or stimulate tumor growth depending on stage, grade, and tumor type. It remains unclear, however, the effect of endometrial-cancer-associated fibroblasts on hormone-driven responses in endometrial cancer. In this study, we investigated the effect of normal and cancer-associated stromal cells from patients with and without endometrial cancer on endometrial tumor growth in response to estradiol (E2) and progesterone (P4). Compared to benign endometrial stromal cells, the low-grade and high-grade cancer-associated stromal cells exhibited a blunted hormone response for proliferation as well as IGFBP1 secretion. Additional analysis of the influence of stromal cells on hormone-driven tumor growth was done by mixing stromal cells from benign, low-grade, or high-grade tumors, with Ishikawa cells for subcutaneous tumor formation. The presence of both benign and high-grade cancer-associated stromal cells increased estradiol-driven xenografted tumor growth compared to Ishikawa cells alone. Low-grade cancer-associated stromal cells did not significantly influence hormone-regulated tumor growth. Addition of P4 attenuated tumor growth in Ishikawa + benign or high-grade stromal cells, but not in Ishikawa cells alone or with low-grade stromal cells. Using an angiogenesis focused real-time array TGFA, TGFB2 and TGFBR1 and VEGFC were identified as potential candidates for hormone-influenced growth regulation of tumors in the presence of benign and high-grade stromal cells. In summary, endometrial-cancer-associated cells responded differently to in vitro hormone treatment compared to benign endometrial stromal cells. Additionally, presence of stromal cells differentially influenced hormone-driven xenograft growth in vivo depending on the disease status of the stromal cells.
癌症相关成纤维细胞已被证明根据阶段、分级和肿瘤类型抑制或刺激肿瘤生长。然而,子宫内膜癌相关成纤维细胞对子宫内膜癌激素驱动反应的影响仍不清楚。在本研究中,我们调查了来自有或没有子宫内膜癌患者的正常和癌症相关基质细胞对子宫内膜肿瘤生长对雌二醇(E2)和孕酮(P4)反应的影响。与良性子宫内膜基质细胞相比,低级别和高级别癌症相关基质细胞对增殖以及IGFBP1分泌的激素反应减弱。通过将来自良性、低级别或高级别肿瘤的基质细胞与石川细胞混合用于皮下肿瘤形成,对基质细胞对激素驱动肿瘤生长的影响进行了进一步分析。与单独的石川细胞相比,良性和高级别癌症相关基质细胞的存在增加了雌二醇驱动的异种移植肿瘤生长。低级别癌症相关基质细胞对激素调节的肿瘤生长没有显著影响。添加P4可减弱石川 + 良性或高级别基质细胞中的肿瘤生长,但在单独的石川细胞或与低级别基质细胞一起时则不然。使用聚焦血管生成的实时阵列TGFA,TGFB2、TGFBR1和VEGFC被确定为在存在良性和高级别基质细胞时激素影响肿瘤生长调节的潜在候选者。总之,与良性子宫内膜基质细胞相比,子宫内膜癌相关细胞对体外激素治疗的反应不同。此外,基质细胞的存在根据基质细胞的疾病状态在体内对激素驱动的异种移植生长有不同影响。