Colorectal cancer (CRC) is the third most common type of cancer worldwide. Currently, surgery, chemotherapy and radiation therapy are the conventional approaches used to treat CRC. However, these therapy strategies cause several side effects. The present study aimed to develop an alternative and more effective treatment approach for patients with CRC. It has been reported that salt‑inducible kinase 2 (SIK2) acts as an oncogene. Therefore, in the present study, the expression levels of SIK2 were determined in CRC cells using western blot analysis and reverse transcription‑quantitative PCR. In addition, SIK2 was knocked down in CRC cells to evaluate its role in cell proliferation, migration, invasion and glycolysis using Cell Counting Kit‑8, wound healing, Transwell assays and glycolysis cell‑based assay kit, respectively. Additionally, the target genes of SIK2 were identified using bioinformatics analysis, while SIK2 overexpression experiments were carried out to determine whether SIK2 could regulate CRC cell malignant behavior and glycolysis. The results revealed that SIK2 was upregulated in CRC cells. Furthermore, SIK2 knockdown attenuated CRC cell proliferation, migration, invasion and glycolysis. Bioinformatics analysis predicted that SIK2 could interact with tripartite motif containing 28 (TRIM28), while TRIM28 overexpression could reverse the effects of SIK2 silencing on cell proliferation, migration, invasion and glycolysis. This finding indicated that the aforementioned effects of SIK2 were mediated by regulating TRIM28. In conclusion, the findings of the present study suggested that SIK2 may be involved in CRC carcinogenesis and glycolysis by regulating TRIM28 expression. These findings could provide a novel approach to targeted therapy and clinical diagnosis of CRC in the future.

中文翻译：

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盐诱导激酶 2 在结直肠癌细胞恶性行为和糖酵解中的作用。

结直肠癌 (CRC) 是全球第三大最常见的癌症类型。目前，手术、化学疗法和放射疗法是用于治疗CRC的常规方法。然而，这些治疗策略会引起一些副作用。本研究旨在为CRC患者开发一种替代且更有效的治疗方法。据报道，盐诱导激酶 2 (SIK2) 是一种致癌基因。因此，在本研究中，使用蛋白质印迹分析和逆转录定量 PCR 测定 CRC 细胞中 SIK2 的表达水平。此外，SIK2 在 CRC 细胞中被敲低，以评估其在细胞增殖、迁移、侵袭和糖酵解中的作用，分别使用 Cell Counting Kit-8、伤口愈合、Transwell 检测和基于糖酵解细胞的检测试剂盒。此外，通过生物信息学分析鉴定SIK2的靶基因，同时进行SIK2过表达实验以确定SIK2是否可以调节CRC细胞恶性行为和糖酵解。结果显示SIK2在CRC细胞中上调。此外，SIK2 敲低减弱了 CRC 细胞增殖、迁移、侵袭和糖酵解。生物信息学分析预测SIK2可以与含有28的三方基序（TRIM28）相互作用，而TRIM28过表达可以逆转SIK2沉默对细胞增殖、迁移、侵袭和糖酵解的影响。这一发现表明SIK2的上述作用是通过调节TRIM28介导的。综上所述，本研究结果表明SIK2可能通过调节TRIM28的表达参与CRC的癌变和糖酵解。这些发现可能为未来CRC的靶向治疗和临床诊断提供一种新方法。