Related Experiment Video
Updated: Dec 19, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LncNORAD interference inhibits tumor growth and lung cancer cell proliferation, invasion and migration by
1Department of Thoracic Surgery, Shanghai Key Laboratory of Clinical Geriatric Medicine, HuaDong Hospital, FuDan University, Shanghai, China. Shenxy2019@yeat.net.
Objective:
Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer, with an unfavorable prognosis of 5-year survival rates. It is of great clinical significance to further search for more efficacious and novel targets for diagnosis and therapeutic strategies. This study aimed at clarifying the role of long non-coding RNA (lncRNA) NORAD in proliferation, invasion and migration and tumor growth of NSCLC.
Materials And Methods:
In this study, mRNA levels of lncRNA NORAD were examined by RT-PCR. CCK-8 assay was applied to test cell viability. Furthermore, wound healing assay and transwell assay were performed to detect the migration and invasion of A549 cells, respectively. Immunohistochemistry was applied to assess the levels of CXC chemokine receptor (CXCR) 4 and CXC chemokine ligand (CXCL) 12. Mice models of NSCLC in vivo were exploited to further examine the potential role of NORAD in tumor growth. Key proteins related to Ras homolog gene family member A (RhoA) GTPase/Rho-associated kinase (RhoA/ROCK) pathway were determined by Western blot.
Results:
NORAD has elevated the levels in NSCLC tissues and cells. NORAD interference dramatically inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion by downregulating CXCR4 and CXCL12 expression. RhoA/ROCK signaling pathway was activated in NSCLC.
Conclusions:
This study revealed that the downregulation of lncRNA NORAD could slow down the progression of NSCLC by regulating CXCR4 and RhoA/ROCK signaling pathway.
Insights
Downregulating long non-coding RNA NORAD inhibits non-small cell lung cancer (NSCLC) progression. This study shows NORAD interference suppresses tumor growth and metastasis by affecting CXCR4 and the RhoA/ROCK pathway.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Non-small cell lung cancer (NSCLC) presents a significant clinical challenge due to poor survival rates.
- Identifying novel diagnostic and therapeutic targets is crucial for improving NSCLC outcomes.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
Purpose of the Study:
- To investigate the role of the lncRNA NORAD in the proliferation, invasion, migration, and tumor growth of NSCLC.
- To elucidate the underlying molecular mechanisms involving CXCR4, CXCL12, and the RhoA/ROCK pathway.
Main Methods:
- Quantitative real-time PCR (RT-PCR) to measure NORAD mRNA levels.
- Cell viability assays (CCK-8), wound healing, and Transwell assays to assess proliferation and cell migration/invasion.
- Immunohistochemistry and Western blot to analyze protein expression (CXCR4, CXCL12, RhoA/ROCK pathway components).
- In vivo NSCLC mouse models to evaluate NORAD's effect on tumor growth.
Main Results:
- NORAD expression was significantly elevated in NSCLC tissues and cells.
- Interference with NORAD markedly inhibited tumor growth and suppressed NSCLC cell proliferation, migration, and invasion.
- NORAD downregulation led to decreased expression of CXCR4 and CXCL12.
- The RhoA/ROCK signaling pathway was found to be activated in NSCLC.
Conclusions:
- Downregulation of lncRNA NORAD can impede NSCLC progression.
- NORAD influences NSCLC by regulating CXCR4 and the RhoA/ROCK signaling pathway.
- Targeting NORAD may offer a potential therapeutic strategy for NSCLC.
Related Concept Videos
lncRNA - Long Non-coding RNAs
Inhibition of Cdk Activity
Small GTPases - Ras and Rho
Three regulatory proteins control their activity:
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Experimental RNAi
Abnormal Proliferation

