scholarly journals miR-621 May Suppress Cell Proliferation via Targeting lncRNA SNHG10 in Acute Myeloid Leukemia

2021 ◽  
Vol Volume 13 ◽  
pp. 2117-2123
Author(s):  
Shishan Xiao ◽  
Yan Zha ◽  
Hongqian Zhu
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Suppress Cell Proliferation ◽  
Acute Myeloid

scholarly journals MIR-140 TARGETS LNCRNA DNAJC3-AS1 TO SUPPRESS CELL PROLIFERATION IN ACUTE MYELOID LEUKEMIA

2022 ◽  
Vol 14 (1) ◽  
pp. e2022005
Author(s):  
Hong Li ◽  
Kehong Bi ◽  
Saran Feng ◽  
Yan Yan Wang ◽  
Chuansheng Zhu
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Cancer Biology ◽  
Direct Interaction ◽  
Subcellular Location ◽  
Subcellular Fractionation ◽  
Suppress Cell Proliferation ◽  
Acute Myeloid

Objectives：MiR-140 and DNAJC3-AS1 have been proven to play critical roles in cancer biology, while their participations in acute myeloid leukemia (AML) are unclear. This study aimed to explore the role of miR-140 and DNAJC3-AS1 in AML. Methods：Analysis of the expression of DNAJC3-AS1 and miR-140 was done with RT-qPCR. The role of DNAJC3-AS1 and miR-140 in the expression of each other was explored with overexpression assay. The direct interaction between DNAJC3-AS1 and miR-140 was analyzed with RNA pull-down assay. The subcellular location of DNAJC3-AS1 was explored with cellular subcellular fractionation assay. Cell proliferation analysis was done with BrdU assay. Results：AML patients showed increased expression of DNAJC3-AS1 and decreased expression of miR-140. DNAJC3-AS1 was detected in both nuclear and cytoplasm samples, and a direct interaction between DNAJC3-AS1 and miR-140 was observed.   Discussion：Reduced expression of DNAJC3-AS1 was observed after miR-140 overexpression in AML cells. DNAJC3-AS1 increased cell proliferation and inhibited the role of miR-140 in suppressing cell proliferation. Conclusion：In conclusion, miR-140 may target DNAJC3-AS1 to suppress cell proliferation in AML.

AML-327: Plasmacytoid Dendritic Cell Proliferation Associated with Acute Myeloid Leukemia: A Case Report

2021 ◽  
Vol 21 ◽  
pp. S306
Author(s):  
Irina Panovska-Stavridis ◽  
Nevenka Ridova ◽  
Simona Stojanovska ◽  
Sanja Trajkova ◽  
Aleksandra Pivkova-Veljanovska ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Case Report ◽  
Dendritic Cell ◽  
Myeloid Leukemia ◽  
Plasmacytoid Dendritic Cell ◽  
Acute Myeloid

Effect of Down-Regulation of miR-23b-3p on the Differentiation of Acute Myeloid Leukemia via Wilms Cancer Gene 1

2021 ◽  
Vol 11 (7) ◽  
pp. 1377-1382
Author(s):  
Lixia Cao ◽  
Jing Zhang ◽  
Huijuan Ren ◽  
Yanqiu Han
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Morphological Changes ◽  
Hot Spot ◽  
Luciferase Assay ◽  
Luciferase Reporter ◽  
Down Regulation ◽  
Blank Group ◽  
Acute Myeloid

miRNA has always been a hot spot research. We assessed the effect of down-regulation of miR-23b-3p on the differentiation of acute myeloid leukemia (AML). Human AML cell line U937 was divided into blank group, NC group and miR-23b-3p low expression group (transfected with miR-23b-3p inhibitor) and miR-23b-3p followed by analysis of WT1 level and relationship between miR-23b-3p and WT1 by dual luciferase reporter assay. All-trans retinoic acid is used to induce differentiation, and then the morphological changes of cells and CD11b level were detected. When miR-23b-3p level was reduced, WT1 mRNA and protein level was also decreased. Dual luciferase assay showed that miR-23b-3p bound to WT1 3’-UTR. Inhibition of miR-23b-3p significantly decreased cell proliferation. Swiss Giemsa staining showed that most of cells were in the differentiation stage with low miR-23b-3p expression. The differentiation marker CD11b was significantly higher than other groups, indicating that low miR-23b-3p expression can promote cell differentiation and reduce cell proliferation to a certain extent. Under low miR-23b-3p expression, the positive rate of CD11b was significantly increased. Down-regulating miR-23b-3p can inhibit WT1 to a certain extent and promote the differentiation of AML, which provides a guidance for the gene-level treatment of AML.

scholarly journals Knockdown of Long Noncoding RNA HOXA-AS2 Suppresses Chemoresistance of Acute Myeloid Leukemia via the miR-520c-3p/S100A4 Axis

2018 ◽  
Vol 51 (2) ◽  
pp. 886-896 ◽  
Author(s):  
Xiaoya Dong ◽  
Zhigang Fang ◽  
Mingxue Yu ◽  
Ling Zhang ◽  
Ruozhi Xiao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Online Programs ◽  
Acute Myeloid

Background/Aims: Among different molecular candidates, there is growing data to support that long noncoding RNAs (lncRNAs) play a significant role in acute myeloid leukemia (AML). HOXA-AS2 is significantly overexpressed in a variety of tumors and associated with anti-cancer drug resistance, however, little is known regarding the expression and function of HOXA-AS2 in the chemoresistance of AML. In this study, we aimed to determine the role and molecular mechanism of HOXA-AS2 in adriamycin-based chemotherapy resistance in AML cells. Methods: Quantitative real-time PCR was used to detect HOXA-AS2 expression in the BM samples and ADR cell lines, U/A and T/A cells. Furthermore, the effects of HOXA-AS2 silencing on cell proliferation and apoptosis were assessed in vitro by CCK8 and flow cytometry, and on tumor growth in vivo. Furthermore, bioinformatics online programs predicted and luciferase reporter assay were used to validate the association of HOXA-AS2 and miR-520c-3p in AML. Results: In this study, we showed that HOXA-AS2 is significantly upregulated in BM samples from AML patients after treatment with adriamycin-based chemotherapy and in U/A and T/A cells. Knockdown of HOXA-AS2 inhibited ADR cell proliferation in vitro and in vivo and promoted apoptosis. Bioinformatics online programs predicted that HOXA-AS2 sponge miR-520c-3p at 3’-UTR with complementary binding sites, which was validated using luciferase reporter assay and anti-Ago2 RIP assay. HOXA-AS2 could negatively regulate the expression of miR-520c-3p in ADR cells. S100A4 was predicted as a downstream target of miR-520c-3p, which was confirmed by luciferase reporter assay. Conclusion: Our results suggest that HOXA-AS2 plays an important role in the resistance of AML cells to adriamycin. Thus, HOXA-AS2 may represent a therapeutic target for overcoming resistance to adriamycin-based chemotherapy in AML.

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