Abstract：
Ovarian cancer (OC) is the fifth leading cause of women\'s death from cancers. The high mortality rate is attributed to the late presence of the disease and the lack of modern diagnostic tools, including molecular biomarkers. Moreover, OC is a highly heterogeneous disease, which contributes to early treatment failure. Thus, exploring OC molecular mechanisms could significantly enhance our understanding of the disease and provide new treatment options. Chromatin remodeling complexes (CRCs) are ATP-dependent molecular machines responsible for chromatin reorganization and involved in many DNA-related processes, including transcriptional regulation, replication, and reparation. Dysregulation of chromatin remodeling machinery may be related to cancer development and chemoresistance in OC. Some forms of OC and other gynecologic diseases have been associated with mutations in specific CRC genes. Most notably, ARID1A in endometriosis-related OC, SMARCA4, and SMARCB1 in hypercalcemic type small cell ovarian carcinoma (SCCOHT), ACTL6A, CHRAC1, RSF1 amplification in high-grade serous OC. Here we review the available literature on CRCs\' involvement in OC to improve our understanding of its development and investigate CRCs as possible biomarkers and treatment targets for OC.
摘要：
卵巢癌(OC)是女性癌症死亡的第五大原因。高死亡率归因于该疾病的晚期存在和缺乏现代诊断工具，包括分子生物标志物。此外，OC是一种高度异质性的疾病，这有助于早期治疗失败。因此，探索OC分子机制可以显著增强我们对该疾病的认识,并提供新的治疗方案.染色质重塑复合物（CRC）是ATP依赖性分子机器，负责染色质重组并参与许多DNA相关过程。包括转录调控，复制,和赔偿。染色质重塑机制的失调可能与OC的癌症发展和化学抗性有关。某些形式的OC和其他妇科疾病与特定CRC基因的突变有关。最值得注意的是,子宫内膜异位症相关OC中的ARID1A，SMARCA4和SMARCB1在高钙血症型小细胞卵巢癌（SCCOHT）中，ACTL6A,高级别浆液性OC中CHRAC1、RSF1扩增。在这里，我们回顾了有关CRC参与OC的现有文献，以提高我们对其发展的理解，并研究CRC作为OC的可能生物标志物和治疗靶标。
