Programmed cell death 4 and BCR-ABL fusion gene expression are negatively correlated in chronic myeloid leukemia

被引:3
|
作者
Zhang, Xia [1 ]
Liu, Riming [1 ]
Huang, Baohua [1 ]
Zhang, Xiaolu [1 ]
Yu, Weijuan [1 ]
Bao, Cuixia [1 ]
Li, Jie [1 ]
Sun, Chengming [1 ]
机构
[1] Qingdao Univ, Dept Lab Med, Yuhuangding Hosp, 20 Yuhuangding East Rd, Yantai 264000, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
programmed cell death 4; tumor suppressor; expression; chronic myeloid leukemia; BCR-ABL; S6 KINASE PATHWAY; TUMOR-SUPPRESSOR; BETA-CATENIN/TCF; PDCD4; EXPRESSION; DOWN-REGULATION; BLAST CRISIS; CARCINOMA; PROTEIN; CELL-DEATH-4; TRANSLATION;
D O I
10.3892/ol.2016.4942
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Programmed cell death 4 (PDCD4) is a tumor suppressor that inhibits carcinogenesis, tumor progression and invasion by preventing gene transcription and translation. Downregulation of PDCD4 expression has been identified in multiple types of human cancer, however, to date, the function of PDCD4 in leukemia has not been investigated. In the present study, PDCD4 mRNA and protein expression was investigated in 50 patients exhibiting various phases of chronic myeloid leukemia (CML) and 20 healthy individuals by reverse transcription-quantitative polymerase chain reaction and western blot analysis. PDCD4 expression and cell proliferation was also investigated following treatment with the tyrosine kinase inhibitor, imatinib, in K562 cells. The results demonstrated that PDCD4 mRNA and protein expression was decreased in all CML samples when compared with healthy controls, who expressed high levels of PDCD4 mRNA and protein. No significant differences in PDCD4 expression were identified between chronic phase, accelerated phase and blast phase CML patients. In addition, PDCD4 expression was negatively correlated with BCR-ABL gene expression (r=-0.6716; P<0.001). Furthermore, K562 cells treated with imatinib exhibited significantly enhanced PDCD4 expression. These results indicate that downregulation of PDCD4 expression may exhibit a critical function in the progression and malignant proliferation of human CML.
引用
收藏
页码:2976 / 2981
页数:6
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