CLK3 positively promoted colorectal cancer proliferation by activating IL-6/STAT3 signaling.

Colorectal cancer (CRC) poses a significant challenge in oncology due to its increasing global incidence and treatment complexities. This study delved into the role of the dual-specificity protein kinase CLK3 in CRC progression and its potential as a therapeutic target. By analyzing clinical data and experimental models comprehensively, we found that CLK3 expression was markedly elevated in CRC tissues compared to normal colon tissue. High CLK3 levels were associated with advanced clinical stages and poor prognosis in CRC patients, suggesting its utility as a prognostic biomarker. Functional assays demonstrated that CLK3 overexpression boosted CRC cell proliferation and ATP production, whereas genetic CLK3 knockdown hindered cell proliferation in vitro and curbed tumor growth in vivo. Mechanistically, we uncovered that CLK3 positively influenced the IL-6/STAT3 signaling pathway by stabilizing JAK2 protein levels. These findings propose targeting CLK3 signaling as a promising therapeutic approach for CRC. Further investigation into CLK3's molecular mechanisms and clinical implications is necessary to fully harness its potential in managing CRC.