Expression Analysis of PVT1, CCDC26, and CCAT1 Long Noncoding RNAs in Acute Myeloid Leukemia Patients

• Published in: Genetic testing and molecular biomarkers Vol. 22; no. 10; p. 593
• Main Authors: Izadifard, Marzieh, Pashaiefar, Hossein, Yaghmaie, Marjan, Montazeri, Maryam, Sadraie, Maryam, Momeny, Majid, Jalili, Mahdi, Ahmadvand, Mohammad, Ghaffari, Seyed Hamidollah, Mohammadi, Saeed, Alimoghaddam, Kamran, Ghavamzadeh, Ardeshir
• Format: Journal Article
• Language: English
• Published: United States 01-10-2018
• Subjects: Adolescent; Adult; Aged; Case-Control Studies; Female; Humans; Leukemia, Myeloid, Acute - genetics; Leukemia, Myeloid, Acute - metabolism; Male; Middle Aged; Prognosis; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Transcription Factors - genetics; CCAT1; long noncoding RNAs; acute myeloid leukemia; PVT1; CCDC26
• ISSN: 1945-0257
• DOI: 10.1089/gtmb.2018.0143

Recent evidence indicates that the PVT1, CCDC26, and CCAT1 long noncoding RNAs (lncRNAs) are involved in the leukemogenic process. This study quantified the expression levels of the PVT1, CCDC26, and CCAT1 lncRNAs in patients with acute myeloid leukemia (AML) and also correlated their expression levels with the clinicopathological features of the patients.
The expression levels of the PVT1, CCDC26, and CCAT1 lncRNAs were analyzed using quantitative reverse transcription-polymerase chain reaction of bone marrow specimens obtained from 86 AML patients, 48 AML-M3 patients, and 40 normal controls.
No differences were found between the combined AML patient populations and the healthy controls with respect to the expression levels of PVT1, CCDC26, and CCAT1 (p = 0.35, p = 0.09, and p = 0.77, respectively). However, compared with the controls, the AML-M3 patients had higher PVT1 expression (p = 0.017). Furthermore, high-risk AML-M3 patients manifested higher expression levels of PVT1 than low- and intermediate-risk groups. In addition, distinctive CCDC26 and CCAT1 expression levels were observed among patients with different French-American-British subtypes (p = 0.001 for CCDC26 and p = 0.013 for CCAT1). Compared with the healthy controls, AML-M4 and M5 had higher CCAT1 expression (p = 0.04) and AML-M2 and AML-M4/M5 patients had higher CCDC26 expression (p < 0.001 and p = 0.02, respectively). In addition, different patterns of CCDC26 expression were found among the different cytogenetic risk subtypes (p = 0.005). Finally, patients with intermediate cytogenetic risk showed higher CCDC26 expression levels.
The differential expression of the PVT1, CCDC26, and CCAT1 lncRNAs in different AML subtypes suggests that the deregulation of these transcripts may function in the multistep leukemogenic process and that they may serve as new therapeutic targets for this malignancy.