Expression and clinical significance of VRK1 in diffuse large B-cell lymphoma

Acta Universitatis Medicinalis Anhui 2020 09 v.55 1440-1445     font:big middle small

Found programs:

Authors:Zhong Xiaomin; Liu Hua; Jiang Chao

Keywords:vaccinia-related kinase 1;diffuse large B cell lymphoma;clinicopathological features;prognosis;cell proliferation;apoptosis

DOI:10.19405/j.cnki.issn1000-1492.2020.09.024

〔Abstract〕 Objective To investigate the expression of vaccinia-related kinase 1(VRK1) in diffuse large B cell lymphoma(DLBCL) and its relationship with clinicopathology and prognosis, and its effect on the apoptosis of DLBCL cells. Methods RT PCR was used to detect the mRNA expression of VRK1 in 98 cases of DLBCL tissues and 62 cases of reactive hyperplasia lymphoid(RHL) lymph nodes. Western blot was performed on normal B cell immortalized cell lines HMy2.CIR and DLBCL cell lines including SU-DHL-4, OCI-Lyl9, OCI-Ly3, VAL, SU-DHL-2 and SU-DHL-6 to detect VRK1 protein expression, and VRK1 expression was analyzed based on DLBCL gene chip expression data in visualization software GEPIA and TCGA database. The relationship between VRK1 expression and clinicopathological features of patients with DLBCL was analyzed. The prognosis of patients with high VRK1 expression and low VRK1 expression was compared. RT PCR was used to detect the expression of DNA repair pathway-related proteins XRCC3 and CDC20 mRNA expression in DLBCL tissues, and to compare the co-expression relationship among VRK1, XRCC3 and CDC20. The silencing of VRK1-stable DLBCL cell line was constructed, and the proliferation and apoptosis ability of cells were detected by soft agar colony formation assay and Annexin V-FITC/PI double labeling assay. Results VRK1 was highly expressed in both DLBCL tissues and cells. VRK1 expression was associated with Ann Arbor staging and immunophenotyping in patients with DLBCL. The 5-year overall survival rate of patients with high VRK1 expression was lower than that of VRK1 low expression group. There was positive co-expression among VRK1, XRCC3 and CDC20. Silencing expression of VRK1 inhibited the proliferation of OCI-Ly3 cells and promoted the apoptosis of OCI-Ly3 cells. Conclusion Silencing VRK1 shows strong anti-tumor potential and has certain clinical significance. It provides new ideas and theoretical basis for future clinical diagnosis, prognosis and molecular targeted therapy of DLBCL based on VRK1.