The Effect of KCTD5 on the Proliferation of Human Acute Monocytic Leukemia U937 cells
Ma Lan, Wang Siheng, Wu Qiong, Xu Tian, He Licai, Lü Jianxin*
KCTD5 is a member of the potassium ion channel tetramer domain (KCTD) protein family. It is reported that KCTD5 may act as an adaptor of Cullin3, while the mechanism in acute myeloid leukemia (AML) remains unknown. The mRNA levels of KCTD5 were negatively correlated with the survival of AML patients by analyzing the data in The Cancer Of Genome Atlas (TCGA) database. The protein levels of KCTD5 in AML cell lines were significantly higher than that in normal peripheral blood mononuclear cells by Western blot. KCTD5 was knocked down by shRNA interference technology and the effect of KCTD5 on the proliferation of human acute monocytic leukemia U937 cells was studied in this paper. The effects of KCTD5 on the growth and viability, cell morphology, cell cycle distribution and cycle-related protein expressions of U937 cells were detected by CCK8 assay, trypan blue exclusion assay, Wright’s staining, PI staining and Western blot, respectively. Our results showed that knockdown of KCTD5 could significantly inhibit the growth of U937 cells, while cell viability did not change obviously. Microscopic examination revealed that knockdown of KCTD5 significantly increased the volume of U937 cells, and the ratio of chromatin condensation and multinuclear cell also increased. Knockdown KCTD5 could increase the proportion of cells in G2/M phase by flow cytometry. The phosphorylation level of Cdk1Tyr15 was decreased and the expression of Cyclin B1 was increased by KCTD5 knockdown. Our results indicated that knockdown of KCTD5 could inhibit the proliferation of human acute monocytic leukemia U937 cells and induce cell cycle arrest at G2/M phase in U937 cells by dephosphorylation of Cdk1Tyr15.
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