Cancer stem cells (CSCs) are the main cause of tumor generation, recurrence, metastasis, and therapy failure in various malignancies including colorectal cancer (CRC). Accumulating evidence suggests that tumor cells can acquire CSC characteristics through the epithelial-mesenchymal transition (EMT) process. However, the molecular mechanism of CSCs remains unclear. OCT4B1 is a transcript of OCT4, which is initially expressed in embryonic stem and carcinoma cells, and is involved in the regulation and maintenance of an undifferentiated state of stem cells. In this study, three-dimensional (3D) microspheres were confirmed as CRC stem cells. Compared with that of parental cells, their self-renewal ability was significantly increased, and OCT4B1 expression was increased and promoted the EMT process. The knockdown of OCT4B1 decreased the self-renewal of CSCs and reversed EMT. Moreover, OCT4B1 induced the expression of Polo-like kinase 1 (PLK1), which is a key regulator of EMT in tumor cells. Further examination showed that OCT4B1 regulated the miR-8064/PLK1 balance to exert its function. Taken together, our data suggest that OCT4B1 may be involved in regulating the self-renewal of colorectal CSCs through EMT, which is at least partially due to the miR-8064/PLK1 balance. This study indicates that OCT4B1 is a potential therapeutic target for CRC by targeting CSCs.

癌症干细胞（CSC）是包括大肠癌（CRC）在内的各种恶性肿瘤中肿瘤产生，复发，转移和治疗失败的主要原因。越来越多的证据表明，肿瘤细胞可以通过上皮-间质转化（EMT）过程获得CSC特征。但是，CSCs的分子机制仍不清楚。OCT4B1是OCT4的转录本，最初在胚胎干细胞和癌细胞中表达，并参与干细胞未分化状态的调节和维持。在这项研究中，三维（3D）微球被确认为CRC干细胞。与亲代细胞相比，它们的自我更新能力显着增强，OCT4B1表达增加并促进了EMT过程。OCT4B1的组合降低了CSC的自我更新并逆转了EMT。此外，OCT4B1诱导了Polo样激酶1（PLK1）的表达，这是肿瘤细胞中EMT的关键调节因子。进一步检查表明，OCT4B1调节miR-8064 / PLK1平衡以发挥其功能。两者合计，我们的数据表明，OCT4B1可能参与通过EMT调节结直肠CSC的自我更新，这至少部分归因于miR-8064 / PLK1平衡。这项研究表明，通过靶向CSC，OCT4B1是CRC的潜在治疗靶标。我们的数据表明，OCT4B1可能参与通过EMT调控结直肠CSC的自我更新，这至少部分归因于miR-8064 / PLK1平衡。这项研究表明，通过靶向CSC，OCT4B1是CRC的潜在治疗靶标。我们的数据表明，OCT4B1可能参与通过EMT调控结直肠CSC的自我更新，这至少部分归因于miR-8064 / PLK1平衡。这项研究表明，通过靶向CSC，OCT4B1是CRC的潜在治疗靶标。