Journal
MOLECULAR CARCINOGENESIS
Volume 61, Issue 6, Pages 572-586Publisher
WILEY
DOI: 10.1002/mc.23403
Keywords
autophagy; colorectal cancer; immunohistochemistry; prognosis; STAT3; STK25; survival
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Funding
- National Natural Science Foundation of China [82173218, 82171720, 81872022, 81672439]
- Beijing Natural Science Foundation [5202008, 7162039]
- Capital's Funds for Health Improvement and Research [CFH2018-2-2153]
- Beijing Hospitals Authority Clinical Medicine Development of Special Funding Support [ZYLX202116]
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This study found that STK25 plays a crucial role in colorectal cancer and inhibits autophagy by activating the JAK2/STAT3 pathway, providing a potential indicator for therapies targeting CRC.
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.
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