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.
RAO Chun-Bao,LUO Dong,LIN Zi-Tian et al. Expression of long non-coding RNA linc00467 in childhood acute myeloid leukemia and its role in drug resistance[J]. CJCP, 2020, 22(7): 734-738.
RAO Chun-Bao,LUO Dong,LIN Zi-Tian et al. Expression of long non-coding RNA linc00467 in childhood acute myeloid leukemia and its role in drug resistance[J]. CJCP, 2020, 22(7): 734-738.
Ramos NR, Mo CC, Karp JE, et al. Current approaches in the treatment of relapsed and refractory acute myeloid leukemia[J]. J Clin Med, 2015, 4(4):665-695.
[3]
Okazaki Y, Furuno M, Kasukawa T, et al. Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs[J]. Nature, 2002, 420(6915):563-573.
[4]
Chen L, Hu N, Wang C, et al. HOTAIRM1 knockdown enhances cytarabine-induced cytotoxicity by suppression of glycolysis through the Wnt/β-catenin/PFKP pathway in acute myeloid leukemia cells[J]. Arch Biochem Biophys, 2020, 680:108244.
[5]
Wang D, Zeng T, Lin Z, et al. Long non-coding RNA SNHG5 regulates chemotherapy resistance through the miR-32/DNAJB9 axis in acute myeloid leukemia[J]. Biomed Pharmacother, 2020, 123:109802.
[6]
Sun H, Sun Y, Chen Q, et al. LncRNA KCNQ1OT1 contributes to the progression and chemoresistance in acute myeloid leukemia by modulating Tspan3 through suppressing miR-193a-3p[J]. Life Sci, 2020, 241:117161.
[7]
Atmadibrata B, Liu PY, Sokolowski N, et al. The novel long noncoding RNA linc00467 promotes cell survival but is down-regulated by N-Myc[J]. PLoS One, 2014, 9(2):e88112.
[8]
Ding H, Luo Y, Hu K, et al. Linc00467 promotes lung adenocarcinoma proliferation via sponging miR-20b-5p to activate CCND1 expression[J]. Onco Targets Ther, 2019, 12:6733-6743.
[9]
Jiang W, Cheng X, Wang T, et al. LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma[J]. J Gene Med, 2020, 22(3):e3134.
[10]
Li GC, Xin L, Wang YS, et al. Long intervening noncoding 00467 RNA contributes to tumorigenesis by acting as a competing endogenous RNA against miR-107 in cervical cancer cells[J]. Am J Pathol, 2019, 189(11):2293-2310.
Yang J, Liu Y, Mai X, et al. STAT1-induced upregulation of LINC00467 promotes the proliferation migration of lung adenocarcinoma cells by epigenetically silencing DKK1 to activate Wnt/β-catenin signaling pathway[J]. Biochem Biophys Res Commun, 2019, 514(1):118-126.
[13]
Wang X, Liu H, Shen K, et al. Long intergenic non-coding RNA 00467 promotes lung adenocarcinoma proliferation, migration and invasion by binding with EZH2 and repressing HTRA3 expression[J]. Mol Med Rep, 2019, 20(1):640-654.
[14]
Cai K, Li T, Guo L, et al. Long non-coding RNA LINC00467 regulates hepatocellular carcinoma progression by modulating miR-9-5p/PPARA expression[J]. Open Biol, 2019, 9(9):190074.
[15]
Zheng Y, Nie P, Xu S. Long noncoding RNA linc00467 plays an oncogenic role in hepatocellular carcinoma by regulating the miR-18a-5p/NEDD9 axis[J]. J Cell Biochem, 2020, 121(5-6):3135-3144.
[16]
Zhang A, Zhao JC, Kim J, et al. LncRNA HOTAIR enhances the androgen-receptor-mediated transcriptional program and drives castration-resistant prostate cancer[J]. Cell Rep, 2015, 13(1):209-221.
[17]
Yang F, Huo XS, Yuan SX, et al. Repression of the long noncoding RNA-LET by histone deacetylase 3 contributes to hypoxia-mediated metastasis[J]. Mol Cell, 2013, 49(6):1083-1096.
[18]
Kühnl A, Kaiser M, Neumann M, et al. High expression of IGFBP2 is associated with chemoresistance in adult acute myeloid leukemia[J]. Leuk Res, 2011, 35(12):1585-1590.
