Song Guo-Qing, Zhao Yi
Department of Pancreas and Breast Surgery, Shengjing Hospital of China Medical University, Heping, Shenyang, Liaoning 110004, P.R. China.
Oncol Rep. 2015 Feb;33(2):669-74. doi: 10.3892/or.2014.3619. Epub 2014 Nov 24.
Breast cancer is the leading cause of cancer-related death in women. Kisspeptin-10 (KP-10) is a shorter fragment of KISS1. In the present study, we demonstrated the antitumor effects of KP-10 on human breast cancer cell lines, MDA-MB-231 and MDA-MB-157, both in vitro and in vivo. KP-10 was observed to induce apoptosis and inhibit the mobility of MDA-MB-231 and MDA-MB-157 cells. Correspondingly, KP-10 suppressed tumor growth in established xenograft tumor models and improved the survival rate of tumor-bearing mice. The formation of intratumoral microvessels was inhibited following treatment with KP-10. Finally, we confirmed that KP-10 inhibited cell mobility via epithelial-mesenchymal transition (EMT). Overall, the present study demonstrated that KP-10 suppressed breast cancer and human umbilical vein endothelial cell (HUVEC) growth both in vivo and in vitro. KP-10 is a novel regulator of EMT in breast cancer cells. However, additional studies are needed to confirm these results in other cell types.
乳腺癌是女性癌症相关死亡的主要原因。 kisspeptin-10（KP-10）是KISS1的较短片段。在本研究中，我们在体外和体内均证明了KP-10对人乳腺癌细胞系MDA-MB-231和MDA-MB-157的抗肿瘤作用。观察到KP-10可诱导MDA-MB-231和MDA-MB-157细胞凋亡并抑制其迁移。相应地，KP-10在已建立的异种移植肿瘤模型中抑制肿瘤生长，并提高荷瘤小鼠的存活率。用KP-10处理后，肿瘤内微血管的形成受到抑制。最后，我们证实KP-10通过上皮-间质转化（EMT）抑制细胞迁移。总体而言，本研究表明KP-10在体内和体外均抑制乳腺癌和人脐静脉内皮细胞（HUVEC）生长。KP-10是乳腺癌细胞中EMT的新型调节因子。然而，需要进一步的研究来在其他细胞类型中证实这些结果。
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