The LINC01260 Functions as a Tumor Suppressor via the miR-562/CYLD/NF-κB Pathway in Non-Small Cell Lung Cancer
Related Experiment Video
Updated: Dec 3, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Yangming Chen1, Yujie Lei2, Jianbin Lin1
1Department of Thoracic Surgery, Shengli Clinical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou, Fujian 350001, People's Republic of China.
Purpose:
Recently, long noncoding RNAs (lncRNAs) have been identified as novel and potential therapeutic targets in various cancer types. Nonetheless, the levels and biological effects of lncRNAs in non-small cell lung cancer (NSCLC) remain largely unknown. In this study, we aimed to identify the effects of lncRNA-LINC01260 throughout the progression of NSCLC and explore the underlying mechanism.
Methods:
Quantitative real-time PCR (qRT-PCR) and Western blot were performed to measure LINC01260, miR-562, and CYLD expression and protein levels. Luciferase reporter assay was employed to investigate the relationship between LINC01260 and miR-562, and miR-562 and CYLD, respectively. The viability and migration of cells were evaluated using CCK-8, colony formation, and transwell assays. The effects of LINC01260 were identified through tumorigenesis in vivo. ELISA was performed to detect the activity of NF-κB and p65 expression.
Results:
In NSCLC tissues and cell lines, LINC01260 expression was downregulated, which corresponded to a lower survival rate of patients with NSCLC. Knockdown of LINC01260 accelerated the proliferation, colony formation, and migration of NSCLC cells. Moreover, downregulation of LINC01260 inhibited apoptosis of NSCLC cells by regulating the expression of Bcl-2 and Bax proteins in vitro. In vivo, the downregulation of LINC01260 promoted tumor growth. miR-562 was identified as the target gene of LINC01260, which was upregulated in NSCLC tumors. Furthermore, CYLD was identified as the target gene of miR-562. The effects of LINC01260 were exerted by regulating CYLD via sponging miR-562. ELISA confirmed that the upregulation of CYLD inhibited NF-κB activity; however, the co-transfection of sh-LINC01260 partly reversed the inhibition. Additionally, CYLD reduced p65 expression; however, downregulation of LINC01260 slightly increased the expression level.
Conclusion:
This study revealed a novel LINC01260/miR-562/CYLD/NF-κB pathway in the pathogenesis of NSCLC and suggested a potential therapeutic target for NSCLC.
Insights
This study reveals that the long noncoding RNA LINC01260 acts as a tumor suppressor in non-small cell lung cancer (NSCLC). Its downregulation promotes cancer progression by affecting the miR-562/CYLD/NF-κB pathway, suggesting LINC01260 as a potential therapeutic target for NSCLC.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Long noncoding RNAs (lncRNAs) are emerging therapeutic targets in cancer.
- The role of lncRNAs in non-small cell lung cancer (NSCLC) is not fully understood.
- This study focuses on lncRNA-LINC01260 in NSCLC pathogenesis.
Purpose of the Study:
- To investigate the effects of lncRNA-LINC01260 in non-small cell lung cancer (NSCLC) progression.
- To elucidate the underlying molecular mechanisms of LINC01260 in NSCLC.
- To identify LINC01260 as a potential therapeutic target for NSCLC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blot to assess gene and protein expression.
- Luciferase reporter assays to confirm molecular interactions.
- Cell viability, migration, and apoptosis assays (CCK-8, colony formation, transwell).
- In vivo tumorigenesis assays and ELISA for NF-κB activity detection.
Main Results:
- LINC01260 was downregulated in NSCLC tissues, correlating with poorer patient survival.
- LINC01260 knockdown enhanced NSCLC cell proliferation, migration, and tumor growth.
- LINC01260 regulates CYLD expression by sponging miR-562, impacting the NF-κB pathway.
Conclusions:
- A novel LINC01260/miR-562/CYLD/NF-κB pathway is identified in NSCLC pathogenesis.
- LINC01260 acts as a tumor suppressor in NSCLC.
- LINC01260 represents a potential therapeutic target for NSCLC treatment.
Related Concept Videos
01:12Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
02:39lncRNA - Long Non-coding RNAs
01:22MicroRNAs
01:22MicroRNAs
02:23Abnormal Proliferation
01:20The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...