Expression of long non-coding RNA linc00467 in childhood acute myeloid leukemia and its role in drug resistance.
- Author:
Chun-Bao RAO
1
;
Dong LUO
;
Zi-Tian LIN
;
Ming-Yu XIE
;
Yuan HU
;
Qi PENG
;
Hua JIANG
;
Zhen-Hong ZHANG
;
Xiao-Mei LU
Author Information
1. Key Laboratory of Genetics and Infectious Diseases, Dongguan Institute of Pediatrics, Dongguan, Guangdong 523327, China. luxm@dgp-institute.com.
- Publication Type:Journal Article
- MeSH:
Cell Proliferation;
Child;
Drug Resistance, Neoplasm;
Humans;
Lentivirus;
Leukemia, Myeloid, Acute;
genetics;
RNA, Long Noncoding;
genetics
- From:
Chinese Journal of Contemporary Pediatrics
2020;22(7):734-738
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study the expression and function of long non-coding RNA linc00467 in childhood acute myeloid leukemia (AML).
METHODS:Bone marrow samples were collected from 5 children with AML who were diagnosed from May 2016 to June 2018. Normal bone marrow samples based on bone marrow examination were collected from 3 children as controls. Quantitative real-time PCR was used to measure the expression of linc00467 in the two groups. A lentivirus system was used to achieve overexpression of linc00467 in AML cells (HL-60) (linc00467 overexpression group), and empty vector expressing green fluorescent protein (GFP) was transfected into AML cells to establish a GFP control group. A lentivirus system was used to insert an interfering sequence into AML cells (sh-linc00467 interfering group), and a random sequence was inserted to establish an sh-NC control group. Cell proliferation and resistance to doxorubicin were observed for all groups.
RESULTS:Compared with the normal control group, the children with AML had a significant increase in linc00467 (P=0.018). Overexpression and interference with linc00467 expression had no significant effect on cell proliferation. Compared with the GFP control group, the linc00467 overexpression group had a significant increase in the viability of HL-60 cells at the adriamycin concentrations of 0.1, 0.2, 0.3, 0.4, and 0.5 μg/mL (P<0.05). Compared with the sh-NC control group, the sh-linc00467 interfering group had a significant reduction in the viability of HL-60 cells at the adriamycin concentrations of 0.1, 0.2, 0.3, 0.4, and 0.5 μg/mL (P<0.05). Compared with the untreated group, the adriamycin treatment group had a significant increase in the expression of linc00467 in HL-60 cells (P<0.05).
CONCLUSIONS:This study reveals the biological function of linc00467 to promote the resistance to adriamycin in AML, which provides a basis for developing new therapeutic drugs for AML.
