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Chronic myeloid leukemia (CML) is a blood cell cancer with increased proliferation of granulocytes. Signal transducers and activators of transcription 3 (STAT3) is an important regulator of CML. To investigate the possible downstream factors of STAT3 and gain more insight into CML-related pathways, this study focused on the superior cervical ganglia protein 10-like protein (SCLIP, or SCG 10-like protein) and analyzed the functions of the STAT3-SCLIP pathway. The effects of STAT3 phosphorylation on SCLIP expression were examined by western blotting. Specific small interfering RNA (siRNA) was then used to knockdown SCLIP in the CML cell line K562 and the expression changes of STAT3 and factors further downstream, namely Bcl-2 and cyclin E1, were detected by RT-qPCR. Cell viability and apoptosis were also analyzed following the knockdown of SCLIP. Results showed a positive association between the phosphorylation of STAT3 and the expression of SCLIP. Knockdown of SCLIP inhibited the viability and induced the apoptosis of K562 cells. Knockdown of SCLIP did not affect the expression of STAT3 mRNA but downregulated the mRNA levels of Bcl-2 and cyclin E1 . In conclusion, the results indicate that SCLIP is a direct downstream factor of STAT3, regulates Bcl-2 and cyclin E1 and mediates the viability and apoptosis of CML cells. Consisting of at least these four factors, the STAT3-SCLIP pathway might play critical roles in the regulation of CML. These data provided a more profound understanding of CML-related pathways.

Expression and functions of the STAT3-SCLIP pathway in chronic myeloid leukemia cells