LINC00665 promotes the progression of acute myeloid leukemia by regulating the miR-4458/DOCK1 pathway
Autor: | Panpan Wang, Ruojin Ma, Xiaojie Li, Yunyun Ma, Sulei Pang, Xiao-yu Yang, Chun-ge Song, Yan Wang |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Male Molecular biology Apoptosis 0302 clinical medicine Cell Movement hemic and lymphatic diseases Gene Regulatory Networks RNA Small Interfering Cancer genetics Base Pairing Cancer Multidisciplinary medicine.diagnostic_test Myeloid leukemia Adhesion Middle Aged rac GTP-Binding Proteins Gene Expression Regulation Neoplastic Leukemia Myeloid Acute 030220 oncology & carcinogenesis Interferon Regulatory Factors Disease Progression Medicine Female RNA Long Noncoding Signal Transduction Adult Cell biology Science HL-60 Cells Biology Article 03 medical and health sciences Western blot Cell Line Tumor medicine Genetics Cell Adhesion Gene silencing Humans Cell adhesion neoplasms Aged Cell Proliferation RNA MicroRNAs 030104 developmental biology Cell culture Case-Control Studies Cancer research |
Zdroj: | Scientific Reports, Vol 11, Iss 1, Pp 1-16 (2021) Scientific Reports |
ISSN: | 2045-2322 |
Popis: | This study aimed to explore the role of LINC00665, miR-4458 and DOCK1 and their interactions in the development of acute myeloid leukemia (AML). The relative expression of LINC00665, miR-4458 and DOCK1 in AML samples was measured using qRT-PCR, and the protein level of DOCK1 in AML cell lines was examined using western blot. CCK8, BrdU, transwell, cell adhesion, and caspase-3 activity assays were carried out to evaluate the viability, proliferation, migration, adhesion, and apoptosis of AML cells, respectively. Luciferase reporter, RIP, and RNA pull-down assays were also performed to confirm the target relationship among LINC00665, miR-4458 and DOCK1. Findings revealed that LINC00665 and DOCK1 were aberrantly overexpressed in AML tissues and that the expression of miR-4458 was low in AML tissues. Silencing LINC00665 or DOCK1 presented significant restriction to the proliferation, migration and adhesion of AML cells. Apart from that, it was found that inhibiting miR-4458 could enhance the proliferation, migration and adhesion of AML cells but suppress the apoptosis of AML cells. Experimental results also indicated that LINC00665 exerted its positive function on AML cells by sponging miR-4458 and that miR-4458 influenced the progression of AML cells by targeting DOCK1 directly. Overall, this finding not only provided a novel molecular pathway for the diagnosis and treatment of AML but also showed that LINC00665 could enhance the progression of AML by regulating the miR-4458/DOCK1 pathway. |
Databáze: | OpenAIRE |
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