癌症是人类所遇到的各种疾病中导致死亡的主要原因。癌症并非单一实体，它包括许多不同类型和亚型，需要不同的治疗方案。在过去的十年中，癌症治疗取得了几个里程碑式的成就，例如特定的靶向药物或激活沉睡的抗肿瘤免疫反应。这些里程碑式的成就导致某些癌症患者产生了显著的积极临床反应，以及肿瘤的缩小和生存延长。因此，在无反应患者和复发患者中，癌症发展起来了细胞死亡的内在抵抗机制，通过抗凋亡基因产物的过度表达。同时，多数抵抗性肿瘤已被报道过度表达一个转录因子，阴阳1（YY1），它调控癌细胞对治疗性抗癌细胞毒素的化疗免疫抗性。本文研究了YY1的过度表达与多种抗凋亡基因产物（如B-细胞淋巴瘤2蛋白（Bcl-2）、B-细胞淋巴瘤额外大（Bcl-xL）、髓细胞白血病1蛋白（Mcl-1）和生存素）之间的关系。研究结果表明，这些抗凋亡基因产物在转录、表观遗传、转录后和翻译水平上部分受YY1调控。虽然每个抗凋亡基因产物的靶向治疗已经进行了一些实验和临床测试，但由于其他过度表达的抗凋亡基因产物的补偿作用，这种靶向策略并不有效。相反，通过小干扰RNA（siRNA）、基因编辑或小分子抑制剂直接靶向YY1可以在过度表达YY1的抵抗性癌症中产生更好的治疗效果。

Cancer is a leading cause of death among the various diseases encountered in humans. Cancer is not a single entity and consists of numerous different types and subtypes that require various treatment regimens. In the last decade, several milestones in cancer treatments were accomplished, such as specific targeting agents or revitalizing the dormant anti-tumor immune response. These milestones have resulted in significant positive clinical responses as well as tumor regression and the prolongation of survival in subsets of cancer patients. Hence, in non-responding patients and non-responding relapsed patients, cancers develop intrinsic mechanisms of resistance to cell death via the overexpression of anti-apoptotic gene products. In parallel, the majority of resistant cancers have been reported to overexpress a transcription factor, Yin Yang 1 (YY1), which regulates the chemo-immuno-resistance of cancer cells to therapeutic anticancer cytotoxic agents. The relationship between the overexpression of YY1 and several anti-apoptotic gene products, such as B-cell lymphoma 2 protein (Bcl-2), B-cell lymphoma extra-large (Bcl-xL), myeloid cell leukemia 1 (Mcl-1) and survivin, is investigated in this paper. The findings demonstrate that these anti-apoptotic gene products are regulated, in part, by YY1 at the transcriptional, epigenetic, post-transcriptional and translational levels. While targeting each of the anti-apoptotic gene products individually has been examined and clinically tested for some, this targeting strategy is not effective due to compensation by other overexpressed anti-apoptotic gene products. In contrast, targeting YY1 directly, through small interfering RNAs (siRNAs), gene editing or small molecule inhibitors, can be therapeutically more effective and generalized in YY1-overexpressed resistant cancers.