Autophagy plays a crucial role in colorectal cancer (CRC) development. Our previous study suggested that serine/threonine protein kinase 25 (STK25) regulates aerobic glycolysis in CRC cells. Glycolysis modulates cellular autophagy during tumor growth; however, the role of STK25 in autophagy remains unclear. In this study, we found that STK25 expression was decreased in CRC tissues and CRC patients with high STK25 expression had a favorable prognosis. Functional assays suggested that STK25 inhibition promoted autophagy in CRC cells. Overexpression of STK25 exhibited the opposite effects. Moreover, the results of western blot demonstrated that silencing STK25 induced autophagy by activating the JAK2/STAT3 pathway. Therefore, STK25 could be a potential indicator for therapies targeting the JAK2/STAT3 pathway in CRC.

中文翻译：

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STK25 的下调通过 Janus 激酶 2/信号转导和转录激活剂 3 通路促进结直肠癌中的自噬

自噬在结直肠癌 (CRC) 的发展中起着至关重要的作用。我们之前的研究表明，丝氨酸/苏氨酸蛋白激酶 25 (STK25) 调节 CRC 细胞的有氧糖酵解。糖酵解在肿瘤生长过程中调节细胞自噬；然而，STK25 在自噬中的作用仍不清楚。在本研究中，我们发现结直肠癌组织中 STK25 表达降低，STK25 高表达的结直肠癌患者预后良好。功能测定表明 STK25 抑制促进了 CRC 细胞中的自噬。STK25 的过表达表现出相反的效果。此外，蛋白质印迹的结果表明，沉默 STK25 通过激活 JAK2/STAT3 通路诱导自噬。因此，STK25 可能是针对 CRC 中 JAK2/STAT3 通路的治疗的潜在指标。