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Updated: Nov 9, 2025

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
LncRNA PCAT1 enhances cell proliferation, migration and invasion by miR-508-3p/NFIB axis in diffuse large B-cell
1Department of Hematology, Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), Qingdao, Shandong Province, China. jiandtlgt119780@163.com.
Long non-coding RNA PCAT1 promotes diffuse large B-cell lymphoma (DLBCL) progression by sponging miR-508-3p and upregulating NFIB. This study elucidates PCAT1's regulatory mechanism in DLBCL.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- PCAT1 is a known driver in hepatocellular carcinoma.
- Its regulatory mechanism in diffuse large B-cell lymphoma (DLBCL) is poorly understood.
Purpose of the Study:
- To investigate the role and regulatory mechanism of PCAT1 in DLBCL.
- To explore the relationship between PCAT1, miR-508-3p, and NFIB in DLBCL.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) for gene expression.
- Cell Counting Kit-8 (CCK-8) and Transwell assays for cell behavior.
- Western blot for protein analysis.
- Dual-Luciferase reporter assay for molecular interactions.
Main Results:
- PCAT1 expression is upregulated in DLBCL tissues and associated with clinical stage and IPI score.
- Overexpression of PCAT1 enhances DLBCL cell proliferation, migration, and invasion.
- PCAT1 sponges miR-508-3p, which targets NFIB; both miR-508-3p and NFIB levels are altered in DLBCL.
- MiR-508-3p overexpression inhibits DLBCL progression, an effect reversed by PCAT1.
- NFIB silencing suppresses DLBCL progression, but this effect is diminished by PCAT1 or miR-508-3p manipulation.
Conclusions:
- PCAT1 functions as a competing endogenous RNA (ceRNA) by sponging miR-508-3p.
- This interaction leads to the upregulation of NFIB, promoting DLBCL cell proliferation, migration, and invasion.
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