PMID- 35196780
OWN - NLM
STAT- MEDLINE
DCOM- 20220225
LR  - 20220531
IS  - 0376-2491 (Print)
IS  - 0376-2491 (Linking)
VI  - 102
IP  - 8
DP  - 2022 Mar 1
TI  - [The role and mechanism of lncRNA C9ORF139 targeting miR-24-3P/TAOK1 in 
      regulating the proliferation of acute myeloid leukemia cells].
PG  - 576-583
LID - 10.3760/cma.j.cn112137-20210703-01501 [doi]
AB  - Objective: To investigate the role and mechanism of long non-coding RNA (lncRNA) 
      C9ORF139 targeting micro RNA(miR)-24-3P/TAOK1 in regulating the proliferation of 
      acute myeloid leukemia (AML) cells. Methods: AML cells HL-60 and THP-1 were 
      purchased from the Chinese Academy of Sciences and divided into 4 groups:group A 
      was negative control group (siNC group), group B was interference C9ORF139 group 
      (siC9ORF139 group), group C was siC9ORF139+miR-24-3p inhibitor group, and group D 
      was miR-24-3P+TAOK1 overexpression group (oe-TAOK1 group). Real-time fluorescence 
      quantitative reverse transcription PCR was used to detect the expression levels 
      of AML cell lines of HL-60 and THP-1 in four groups. Cell Counting Kit-8 assay 
      was performed to measure cell proliferation. Flow cytometry was applied to 
      analyze cell apoptosis. Transwell test was applied to detect cell migration and 
      invasion ability. Western blot was used to detect p-serine/threonine kinase 
      (p-raf) and p-mitogen activation proteinkinase (p-MEK), p-extracellular 
      regulatory protein kinase (p-ERK) expression. The luciferase reporter gene 
      plasmid was constructed to verify the binding ability of C9ORF139,miR-24-3P and 
      TAOK1.Nude mice were inoculated with subcutaneous tumor cells of HL-60 (group A) 
      and HL-60 (group B). Results: After the C9ORF139 gene was knocked down and 
      cultured for 120 h, The cell proliferation ability (0.62+/-0.02, 0.82+/-0.02), 
      migration ability (0.22+/-0.03, 0.05+/-0.01), invasion ability (0.20+/-0.02, 0.13+/-0.03) 
      of group B were all lower than that of group A (1.30+/-0.02, 1.83+/-0.07; 0.99+/-0.02, 
      0.99+/-0.02; 1.00+/-0.01, 1.00+/-0.01) (all P<0.05). When co-transfected with miR-24-3 
      inhibitor, cell proliferation ability, migration ability and invasion ability 
      were all higher in group B (all P<0.05). When co-transfected with miR-24-3P and 
      oe-TAOK1 plasmid, cell proliferation ability, migration ability and invasion 
      ability were all higher than group B (all P<0.05).When the C9ORF139 gene in the 
      cells was knocked down, the apoptosis level of group B (28.56+/-8.07, 17.74+/-1.91) 
      were higher than those of group A (0.31+/-0.27, 2.49+/-0.33)(all P<0.05); when 
      co-transfected with miR-24-3P inhibitor, the apoptosis level (2.34+/-0.09, 
      3.06+/-0.06) were lower than those in group B (all P<0.05); when co-transfected 
      with miR-24-3P and oe-TAOK1 in the plasmid group, the apoptosis level (2.16+/-1.29, 
      4.80+/-0.37) were also lower than those of group B (all P<0.05). In HL-60 and THP-1 
      cells, when C9ORF139 was not mutated, the luciferase activity of miR-24-3P group 
      was lower than that of the miR-NC group (P<0.05). When the binding site with 
      miR-24-3p in C9ORF139 sequence was mutated, the luciferase activity in miR-24-3p 
      group was equivalent to that in miR-NC group (P>0.05).When TAOK1 was not mutated; 
      the luciferase activity of miR-24-3P group was lower than that of group A 
      (P<0.05). When the binding site with miR-24-3p in TAOK1 sequence was mutated, the 
      luciferase activity in miR-24-3p group was equivalent to that in miR-NC group 
      (P>0.05).When the C9ORF139 gene in HL-60 cells was knocked down and cultured for 
      72 h, the phosphorylation expression levels of Raf, MEK and ERK molecules in 
      group B were significantly lower than those in group A (all P<0.05). By day 14, 
      the tumor volume in the group A was greater than the tumor cell volume in the 
      group B [(284.49+/-57.61) vs (125.70+/-18.64) mm(3), P=0.017]. The tumor weight of 
      HL-60 in group A was heavier than that of group B [(847.80+/-159.36) vs 
      (408.40+/-113.16) mg, P=0.001]. Conclusions: LncRNA C9ORF139 regulates TAOK1 by 
      sponging miR-24-3P to promote the proliferation, invasion and migration of acute 
      myeloid leukemiacell.In vivo experiments have confirmed that the expression of 
      C9ORF139 can promote the growth of subcutaneous tumors in AML nude mice.
FAU - Qin, W
AU  - Qin W
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Cai, X H
AU  - Cai XH
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Han, W M
AU  - Han WM
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Lu, X Z
AU  - Lu XZ
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Chen, M Y
AU  - Chen MY
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Jia, Z X
AU  - Jia ZX
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Liu, J
AU  - Liu J
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Xiao, R
AU  - Xiao R
AD  - Department of Hematology, the Affiliated Changzhou 2nd People's Hospital of 
      Nanjing Medical University, Changzhou 213000, China.
FAU - Qian, S X
AU  - Qian SX
AD  - Department of Hematology, Jiangsu Provincial People's Hospital, Nanjing 210029, 
      China.
LA  - chi
GR  - 81870119, 82170153, 81500103/National Natural Science Foundation of China/
GR  - CJ20210068/Changzhou Science and Technology Plan/
GR  - NMUB201/Nanjing Medical University Science and Technology Development Fund 
      Project/
GR  - QN202035/Changzhou Health Committee Science and Technology Project/
GR  - 2019K002/Youth Fund of Changzhou Second People's Hospital/
PT  - Journal Article
PL  - China
TA  - Zhonghua Yi Xue Za Zhi
JT  - Zhonghua yi xue za zhi
JID - 7511141
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - Cell Proliferation
MH  - *Leukemia, Myeloid, Acute/genetics
MH  - Mice
MH  - Mice, Nude
MH  - *MicroRNAs/genetics/metabolism
MH  - *Protein Serine-Threonine Kinases
MH  - *RNA, Long Noncoding/genetics/metabolism
EDAT- 2022/02/24 06:00
MHDA- 2022/02/26 06:00
CRDT- 2022/02/23 20:22
PHST- 2022/02/23 20:22 [entrez]
PHST- 2022/02/24 06:00 [pubmed]
PHST- 2022/02/26 06:00 [medline]
AID - 10.3760/cma.j.cn112137-20210703-01501 [doi]
PST - ppublish
SO  - Zhonghua Yi Xue Za Zhi. 2022 Mar 1;102(8):576-583. doi: 
      10.3760/cma.j.cn112137-20210703-01501.