期刊
ONCOTARGET
卷 6, 期 2, 页码 1276-1285出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.2626
关键词
chronic lymphocytic leukemia; PTEN; mutation; microRNA
资金
- National Natural Science Foundation of China [30871104, 30971296, 81000216, 81100352, 81170485, 81170486, 81170488, 81370657, 81470328]
- Health Department of Jiangsu Province [K201108]
- Jiangsu Province's Medical Elite Program [RC2011169]
- National Public Health Grand Research Foundation [201202017]
- Priority Academic Program Development of Jiangsu Higher Education Institute [JX10231801]
- Program for Development of Innovative Research Teams in the First Affiliated Hospital of Nanjing Medical University
- Project of National Key Clinical Specialty
- National Science & Technology Pillar Program [2014BAI09B12]
- Jiangsu Provincial Special Program of Medical Science [BL2014086]
We previous found the expression level of PTEN was low in the chronic lymphocytic leukemia (CLL) patients. To assess the pathogenic contribution of the low expression of PTEN, we determined PTEN-regulating miRNA interference, PTEN promoter methylation and PTEN gene mutation condition in CLL. One hundred and fifty-four previously untreated CLL patients and 200 cases of healthy controls were sequenced in exons 5-9 of PTEN. None of single nucleotide polymorphism site or mutation was detected in the coding sequences of those exons. Methylation of PTEN promoter was found in one (1.33%) of the 75 patients with CLL, but none of the 25 age-matched control subjects. We found that PTEN was a potential target of miR-26a and miR-214, which had been confirmed following dual-luciferase reporter assays, reverse transcription polymerase chain reaction and Western blotting. High expression of miR-26a was associated with advanced Binet stage (P=0.012), p53 aberrations (P=0.014) and inferior time to first treatment (P=0.038), and high expression of miR-214 was only associated with p53 aberrations (P=0.041). Inhibition of miR-26a or miR-214 could induce more apoptosis in primary cultured CLL cells. These findings support miR-26a and miR-214 down-regulate expression of PTEN in CLL, but not PTEN mutation or promoter methylation.
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