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首页> 外文期刊>Life sciences >Mitochondrial targeting drug lonidamine triggered apoptosis in doxorubicin-resistant HepG2 cells.
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Mitochondrial targeting drug lonidamine triggered apoptosis in doxorubicin-resistant HepG2 cells.

机译：线粒体靶向药物lonidamine触发了对阿霉素耐药的HepG2细胞的凋亡。

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摘要

Mitochondria play a crucial role in the induction and execution of apoptosis. Accordingly, recent suggestions have been made to use agents that directly act on mitochondria to trigger apoptosis so that drug-sensitive and-resistant tumour cells can be eliminated. To test this hypothesis, human hepatocarcinoma HepG2 and its derivative R-HepG2 with doxorubicin (Dox) resistance as a result of expression of P-glycoprotein were used to investigate the effect of lonidamine (LND), a new mitochondrial targeting drug, on the induction of apoptosis. Results from our study indicate that R-HepG2 cells were more sensitive to LND than parental cells in terms of cytotoxicity determined by alamar blue assay. Cell death induced by LND was associated with the hallmarks of apoptosis such as mitochondrial membrane depolarization, release of cytochrome c, phosphatidyl-serine externalization and DNA fragmentation. Moreover, combined treatment of cells with Dox and LND elicited more cell death. Taken together, our results suggest a potential use of LND as an anti-cancer drug to bypass drug resistance and to trigger tumour destruction through apoptosis in HepG2 and R-HepG2 cells.
机译：线粒体在细胞凋亡的诱导和执行中起着至关重要的作用。因此，最近提出了使用直接作用于线粒体以触发细胞凋亡的试剂的建议，从而可以消除药物敏感性和耐药性的肿瘤细胞。为了验证这一假设，使用了人类肝癌HepG2及其衍生的R-HepG2（由于表达P-糖蛋白而具有对阿霉素（Dox）的耐药性）来研究新型线粒体靶向药物lonidamine（LND）对诱导的影响凋亡。我们的研究结果表明，就通过阿尔玛蓝测定法确定的细胞毒性而言，R-HepG2细胞对LND的敏感性比亲代细胞高。 LND诱导的细胞死亡与凋亡的特征有关，例如线粒体膜去极化，细胞色素c的释放，磷脂酰丝氨酸的外在化和DNA片段化。此外，用Dox和LND联合处理细胞会引起更多的细胞死亡。两者合计，我们的结果表明，LND作为一种抗癌药物可能会绕过耐药性并通过HepG2和R-HepG2细胞的凋亡引发肿瘤破坏，从而具有潜在的用途。

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