Multiple myeloma (MM) is the second most common hematological cancer all over the world. Long non-coding RNA (lncRNA) nuclear-enriched autosomal transcript-1 (NEAT1) have been reported to play important roles in the development and progression of multiple human malignancies like MM. However, the functional role and molecular mechanism of NEAT1 in MM progression still needs more support to identify potential targets of MM. In the present study, we focused on the clinical and biological significance of NEAT1 in MM. We demonstrated that NEAT1 was up-regulated in MM tissues and cell line. NEAT1 silencing significantly inhibited cell proliferation and promoted cell apoptosis in vitro. And we illustrated that miR-485-5p was a direct target of NEAT1 and the effect of down-regulated NEAT1 on MM cells was partially reversed by the miR-485-5p antisense oligonucleotide (ASO-miR-485-5p). Further investigation revealed that ABCB8 directly interacted with miR-485-5p. Similarly, in vivo experiments confirmed that down-regulated NEAT1 inhibited tumor growth and ABCB8 expression. Taken together, our results demonstrate for the first time that NEAT1/miR-485-5p/ABCB8 axis may be a key pathway for the development and progression of MM, and they may provide a novel avenue for targeted therapy.

Download full-text PDF

Source
http://dx.doi.org/10.1080/16078454.2024.2422153DOI Listing

Publication Analysis

Top Keywords

neat1
9
long non-coding
8
non-coding rna
8
multiple myeloma
8
development progression
8
down-regulated neat1
8
rna neat1
4
neat1 promotes
4
promotes multiple
4
myeloma malignant
4

Similar Publications

Background: The SARS-CoV-2 virus's frequent mutations have made disease control with vaccines and antiviral drugs difficult; as a result, there is a need for more effective coronavirus drugs. Therefore, detecting the expression of various diagnostic biomarkers, including ncRNA in SARS-CoV2, implies new therapeutic strategies for the disease.

Aim: Our study aimed to measure NEAT-1, miR-374b-5p, and IL6 in the serum of COVID-19 patients, demonstrating the correlation between target genes to explore the possible relationship between them.

View Article and Find Full Text PDF

Histone Lactylation-Driven YTHDC1 Promotes Hepatocellular Carcinoma Progression via Lipid Metabolism Remodeling.

Cancer Lett

December 2024

Shanghai Center for Systems Biomedicine, Key Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Jiao Tong University, Shanghai, 200240, China. Electronic address:

Lipid metabolism reprogramming is critical for the initiation and progression of hepatocellular carcinoma (HCC). However, how the dysregulation of lipid metabolism contributes to HCC development remains largely unknown. Here, we report that the mA reader YTHDC1-mediated epigenetic regulation of the long noncoding RNA NEAT1 activates stearoyl-CoA desaturase (SCD)-associated lipid metabolic processes during HCC progression.

View Article and Find Full Text PDF

Background: Acute graft-versus-host disease (aGVHD) is a complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT). The role of macrophages as proficient antigen-presenting cells in aGVHD is a prominent area of investigation in contemporary research. The association between long noncoding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) and the macrophage function is of significant interest.

View Article and Find Full Text PDF

HCC cell immune escape is a critical element in the evolution of HCC malignancy. Herein, the regulatory mechanism of lncRNA NEAT1 in regulating HCC immune escape was investigated. Exosomes were isolated from M2 TAMs using ExoQuick-TC.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!