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
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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