{Reference Type}: Journal Article
{Title}: Overexpression of NOP58 Facilitates Proliferation, Migration, Invasion, and Stemness of Non-small Cell Lung Cancer by Stabilizing hsa_circ_0001550.
{Author}: Jiang Y;Cai Y;Bao Y;Kong X;Jin H;
{Journal}: Anticancer Agents Med Chem
{Volume}: 0
{Issue}: 0
{Year}: 2024 Jul 11
{Factor}: 2.527
{DOI}: 10.2174/0118715206293943240615105417
{Abstract}: <B>BACKGROUND: </B>NOP58 ribonucleoprotein (NOP58) is associated with the recurrence of lung adenocarcinoma.<BR><B>OBJECTIVE: </B>Few investigations concentrate on the role of NOP58 in non-small cell lung cancer (NSCLC), which is the focus of our current study.<BR><B>METHODS: </B>Following transfection, the proliferation, migration, and invasion of NSCLC cells were assessed by 5- ethynyl-2'-deoxyuridine (EdU), wound healing, and transwell assays. The percentage of CD9+ cells was evaluated by flow cytometry assay. Based on target genes and binding sites predicted through bioinformatics analysis, a dual-luciferase reporter assay was performed to verify the targeting relationship between hsa_circ_0001550 and NOP58. The effect of NOP58 overexpression on hsa_circ_0001550 stability was gauged using Actinomycin D. The hsa_circ_0001550 and NOP58 expression levels, as well as protein expressions of CD44, CD133, OCT4, and SOX2 in NSCLC cells were determined by quantitative real-time PCR and Western blot, respectively.<BR><B>RESULTS: </B>Hsa_circ_0001550 was remarkably up-regulated in NSCLC cell lines A549 and PC9, silencing of which weakened cell abilities to proliferate, migrate and invade, decreased CD9+ cell ratio, and diminished protein expressions of CD44, CD133, OCT4, and SOX2. NOP58 could bind to hsa_circ_0001550 and stabilize its expression, and NOP58 overexpression partially abrogated hsa_circ_0001550 knockdown-inhibited NSCLC cell proliferation, migration, invasion and stemness.<BR><B>CONCLUSIONS: </B>Overexpression of NOP58 facilitates proliferation, migration, invasion, and stemness of NSCLC cells by stabilizing hsa_circ_0001550, hinting that NOP58 is a novel molecular target for NSCLC therapy.