AIM Despite recent advances in therapeutic strategies, cancer is still a leading cause of mortality worldwide. Mitochondrial dysfunction is implicated in cancer initiation and metastasis, and even in chemo- and radio-resistance. However, the precise role of mitochondria in cancer is crosstalk and controversial. This study is trying to find out the effect of transferring normal mitochondria into the highly aggressive and proliferative MDA-MB-231 cancer cells, and to evaluate the effect of the transfer with/without a combination therapy with cisplatin. MATERIALS AND METHODS Normal mitochondria were isolated from human umbilical cord derived-mesenchymal stem cells. The mitochondria were transferred into the MDA-MB-231 cells, and also into cells with mitochondrial dysfunction induced by rhodamine red 6 (R6G). Cell proliferation and sensitivity of the cells to cisplatin were measured by cell counting after the mitochondria transfer. Also, apoptosis was evaluated by DAPI staining and in situ cell death detection (TdT-mediated dUTP nickend labeling; TUNEL) methods. Migration capability of the cells was studied by transwell assay. KEY FINDINGS Transfer of normal mitochondria into MDA-MB-231 cells increased cell proliferation. However, the transfer of mitochondria enhanced cisplatin-induced apoptosis in MDA-MB-231 cells in which mitochondria were already disrupted. Introduction of normal cell-derived mitochondria into the MDA-MB-231 cells increased their invasive, but decreased the migration potency of the cells in the group with mitochondrial dysfunction (MDA + RG6 + Cisplatin). CONCLUSION The introduction of healthy mitochondria to highly aggressive and proliferative cells would be considered as a new therapeutic modality for some types of cancer.

中文翻译：

---

线粒体特性有助于MDA-MB-231癌细胞的增殖和迁移能力及其对顺铂治疗的反应。

目的尽管最近在治疗策略方面取得了进步，但癌症仍然是全球范围内导致死亡的主要原因。线粒体功能障碍与癌症的发生和转移有关，甚至与化学和放射抗性有关。然而，线粒体在癌症中的确切作用是串扰和有争议的。这项研究试图发现将正常的线粒体转移到高度侵袭性和增殖性的MDA-MB-231癌细胞中的作用，并评估有/无顺铂联合治疗的转移作用。材料与方法从人脐带间充质干细胞中分离出正常的线粒体。线粒体转移到MDA-MB-231细胞中，也转移到若丹明红6（R6G）诱导的具有线粒体功能障碍的细胞中。通过线粒体转移后的细胞计数来测量细胞增殖和细胞对顺铂的敏感性。此外，通过DAPI染色和原位细胞死亡检测（TdT介导的dUTP缺口标记； TUNEL）方法评估凋亡。通过transwell测定法研究细胞的迁移能力。主要发现正常线粒体转移至MDA-MB-231细胞可增加细胞增殖。然而，线粒体的转移增强了顺铂诱导的MDA-MB-231细胞中的线粒体已经被破坏的凋亡。将正常细胞源的线粒体引入MDA-MB-231细胞中可增加其侵袭性，但会降低线粒体功能障碍（MDA + RG6 +顺铂）组中细胞的迁移能力。