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Updated: Sep 28, 2025

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RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
Published on: April 10, 2018
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LncRNA NEAT1 regulate diffuse large B-cell lymphoma by targeting miR-495-3p/PD-L1 axis
Jun Yuan1, Jie Yang1, Ruicang Wang1
1Blood Specialty, Hebei General Hospital, Shijiazhuang, China.
Immunopharmacology and Immunotoxicology
|March 30, 2022
Summary
NEAT1 is overexpressed in diffuse large B-cell lymphoma (DLBCL). Targeting NEAT1 and its downstream molecule miR-495-3p may offer a new therapeutic strategy for DLBCL treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Diffuse large B-cell lymphoma (DLBCL) is a prevalent lymphoid malignancy.
- Long non-coding RNAs (lncRNAs) are implicated in cancer development, including DLBCL.
- This research investigates the specific role of NEAT1 in DLBCL pathogenesis.
Purpose of the Study:
- To elucidate the function of NEAT1 in DLBCL.
- To identify the molecular mechanisms underlying NEAT1's role in DLBCL.
- To explore NEAT1 as a potential therapeutic target or biomarker for DLBCL.
Main Methods:
- Quantitative polymerase chain reaction (RT-qPCR) for mRNA expression analysis.
- Bioinformatic prediction (StarBase, TargetScan) and experimental validation (Dual Luciferase Reporter Assay, RNA pull-down) of targeting relationships.
- Cell viability (CCK-8), apoptosis (flow cytometry), cytotoxicity (LDH release), and protein expression (Western blotting) assays.
Main Results:
- NEAT1 expression is elevated in DLBCL patients and promotes tumor cell viability and proliferation.
- NEAT1 directly targets and downregulates miR-495-3p, a tumor suppressor.
- NEAT1 acts as a molecular sponge for miR-495-3p, leading to the upregulation of PD-L1, a key immune checkpoint molecule.
Conclusions:
- A novel NEAT1/miR-495-3p/PD-L1 signaling axis is identified as a regulator of DLBCL progression.
- NEAT1 inhibition suppresses DLBCL malignancy by restoring miR-495-3p levels and reducing PD-L1 expression.
- NEAT1 represents a promising diagnostic biomarker and therapeutic target for DLBCL.
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