Lyakhovich Alex, Lleonart Matilde E
International Clinical Research Center, St. Anne's University Hospital, Masaryk University, Kamenice 5/A7, 625 00 Brno, Czech Republic ; Institute of Molecular Biology and Biophysics, Novosibirsk, Russia.
Oncology and Pathology Group, Institut de Recerca Hospital Vall d'Hebron, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain.
Oxid Med Cell Longev. 2016;2016:1716341. doi: 10.1155/2016/1716341. Epub 2015 Nov 30.
Cancer stem cells (CSCs) are highly resistant to conventional chemo- and radiotherapeutic regimes. Therefore, the multiple drug resistance (MDR) of cancer is most likely due to the resistance of CSCs. Such resistance can be attributed to some bypassing pathways including detoxification mechanisms of reactive oxygen and nitrogen species (RO/NS) formation or enhanced autophagy. Unlike in normal cells, where RO/NS concentration is maintained at certain threshold required for signal transduction or immune response mechanisms, CSCs may develop alternative pathways to diminish RO/NS levels leading to cancer survival. In this minireview, we will focus on elaborated mechanisms developed by CSCs to attenuate high RO/NS levels. Gaining a better insight into the mechanisms of stem cell resistance to chemo- or radiotherapy may lead to new therapeutic targets thus serving for better anticancer strategies.
癌症干细胞(CSCs)对传统的化疗和放疗方案具有高度抗性。因此,癌症的多药耐药性(MDR)很可能归因于癌症干细胞的抗性。这种抗性可归因于一些旁路途径,包括活性氧和氮物种(RO/NS)形成的解毒机制或自噬增强。与正常细胞不同,正常细胞中RO/NS浓度维持在信号转导或免疫反应机制所需的特定阈值,而癌症干细胞可能会发展出替代途径来降低RO/NS水平,从而导致癌症存活。在本综述中,我们将重点阐述癌症干细胞为降低高RO/NS水平而发展出的详细机制。深入了解干细胞对化疗或放疗的抗性机制可能会带来新的治疗靶点,从而为更好的抗癌策略提供依据。