Human CD133+ hematopoietic progenitor cells (HPCs) are a specific subset of cells that can regulate tumor malignancy. However, the mechanism by which CD133+ HPCs affect the malignancy of human breast cancer has not been reported. CD133+ HPCs were isolated and purified from human umbilical cord blood (UCB). We used in vitro culture of MCF-7 and MDA-MB-231 cell lines, and MCF-7 and MDA-MB-231 cells in nude mice to evaluate whether CD133+ HPCs affected the apoptosis, proliferation, invasion and epithelial mesenchymal transition EMT of breast cancer cells. Co-culture with CD133+ HPCs, but not UCB CD133- cells, promoted the proliferation of human breast cancer MCF-7 and MDA-MB-231 cells, accompanied by reducing in vitro spontaneous apoptosis. Co-administration of these two lines with CD133+ HPCs significantly enhanced the growth of implanted breast cancer in vivo. Furthermore, co-culture with CD133+ HPCs, enhanced the invasion of breast cancer cells, N-cadherin and Vimentin expression, but reduced E-cadherin expression in breast cancer cells. Our study demonstrated that CD133+ HPCs enhance the malignancy of breast cancer cells by attenuating spontaneous apoptosis and promoting the process of epithelial mesenchymal transition. These findings may provide new insights into the role of human CD133+ HPCs in breast cancer pathogenesis. Therefore, CD133+ HPCs may be a new therapeutic target for inhibiting the progression of breast cancer.

中文翻译：

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人CD133阳性造血祖细胞增强乳腺癌细胞的恶性程度

人CD133 +造血祖细胞（HPC）是可以调节肿瘤恶性程度的特定细胞亚群。然而，尚未报道CD133 + HPC影响人类乳腺癌的恶性机制。从人脐带血（UCB）中分离并纯化CD133 + HPC。我们使用体外培养的MCF-7和MDA-MB-231细胞系，以及MCF-7和MDA-MB-231细胞在裸鼠中进行体外培养，以评估CD133 + HPC是否影响细胞的凋亡，增殖，侵袭和上皮间质转化EMT。乳腺癌细胞。与CD133 + HPC共同培养，但不与UCB CD133-细胞共同培养，可促进人乳腺癌MCF-7和MDA-MB-231细胞的增殖，并伴有体外自发凋亡的减少。将这两个系与CD133 + HPC共同给药可显着增强体内植入的乳腺癌的生长。此外，与CD133 + HPC的共培养可增强乳腺癌细胞的侵袭，N-钙黏着蛋白和波形蛋白的表达，但会降低乳腺癌细胞中E-钙黏着蛋白的表达。我们的研究表明，CD133 + HPC通过减弱自发凋亡和促进上皮间充质转化的过程来增强乳腺癌细胞的恶性程度。这些发现可能为人类CD133 + HPC在乳腺癌发病中的作用提供新的见解。因此，CD133 + HPCs可能是抑制乳腺癌进展的新治疗靶点。但会降低乳腺癌细胞中E-钙黏着蛋白的表达。我们的研究表明，CD133 + HPC通过减弱自发凋亡和促进上皮间充质转化的过程来增强乳腺癌细胞的恶性程度。这些发现可能为人类CD133 + HPC在乳腺癌发病中的作用提供新的见解。因此，CD133 + HPCs可能是抑制乳腺癌进展的新治疗靶点。但会降低乳腺癌细胞中E-钙黏着蛋白的表达。我们的研究表明，CD133 + HPC通过减弱自发凋亡和促进上皮间充质转化的过程来增强乳腺癌细胞的恶性程度。这些发现可能为人类CD133 + HPC在乳腺癌发病中的作用提供新的见解。因此，CD133 + HPCs可能是抑制乳腺癌进展的新治疗靶点。