J Cancer 2024; 15(8):2424-2430. doi:10.7150/jca.92202 This issue Cite
Research Paper
1. Department of Hematology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, P R China.
2. Department of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, P R China.
3. Department of Laboratorial Medicine, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, P R China.
4. Clinical Prenatal Diagnosis Center, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, P R China.
5. Zhejiang Provincial Key Lab of Hematopoietic Malignancy, Zhejiang University, Hangzhou, P R China.
Cofilin (CFL1) is one critical member of the actin deploy family (ADF). Overexpression of CFL1 is associated with aggressive features and poor prognosis in malignancies. We evaluated the expression of CFL1 in patients with chronic myeloid leukemia in the chronic phase (CML-CP), acute myelocytic leukemia (AML) and healthy controls. The role of CFL1 in imatinib therapy was also investigated using cell line. We found that the expression of CFL1 was lower in CML patients than that in healthy controls, and was significantly upregulated after imatinib therapy (p<0.05). CML patients with lower CFL1 achieved higher Major molecular response (MMR) rate after 6 months of imatinib therapy (p<0.05). Cofilin, P-cofilin and F-actin, especially branched F-actin were all upregulated after imatinib therapy. The lower CFL1 expression before treatment may predicts a better response to imatinib. Imatinib affects F-actin remodeling in CML patients by regulating CFL1 expression and activity.
Keywords: Chronic myeloid leukemia, Prognostic value, Imatinib mesylate, CFL1, F-actin