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Updated: Jan 22, 2026

Promoter Capture Hi-C: High-resolution, Genome-wide Profiling of Promoter Interactions
Published on: June 28, 2018
Long noncoding LUCAT1 promotes cisplatin resistance of non-small cell lung cancer by promoting IGF-2
1Department of Pharmacy, Yantai Yuhuangding Hospital, Yantai, China. liutao567@163.com.
Objective:
Drug-resistance remains a huge problem in the therapy of malignant tumors including non-small cell lung cancer (NSCLC). Several researches have proved that long noncoding RNAs (lncRNAs) contributes to drug-resistance in NSCLC. LncRNA LUCAT1 was explored to identify how it functions in the cisplatin-resistance of NSCLC patients.
Materials And Methods:
Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect LUCAT1 expression in A549/DDP cells and A549 cells. Then, we conducted cell counting kit-8 (CCK-8) assay and flow cytometric analysis to detect the function of LUCAT1 on the resistance of NSCLC cells to cisplatin. Furthermore, the potential mechanism was explored by mechanism assays.
Results:
LUCAT1 expression of A549/DDP cells was higher than paired A549 cells. Besides, cell apoptosis was inhibited, cell cycle distribution was changed, and resistance to cisplatin was promoted after LUCAT1 was overexpressed in A549 cells. Furthermore, the overexpression of LUCAT1 could upregulate the IGF-2 expression in A549/DDP cells.
Conclusions:
We suggest that LUCAT1 regulates cell cycle, cell apoptosis of NSCLC cells and the resistance to cisplatin through targeting IGF-2 and could be a possible target for NSCLC treatment.
Insights
Long noncoding RNA LUCAT1 promotes cisplatin resistance in non-small cell lung cancer (NSCLC) by affecting cell cycle and apoptosis. Targeting LUCAT1 may offer a new therapeutic strategy for NSCLC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Drug resistance is a significant challenge in treating non-small cell lung cancer (NSCLC).
- Long noncoding RNAs (lncRNAs) have emerged as key regulators in NSCLC drug resistance.
- LncRNA LUCAT1's role in cisplatin resistance warrants further investigation.
Purpose of the Study:
- To investigate the function of lncRNA LUCAT1 in cisplatin resistance in NSCLC.
- To explore the underlying molecular mechanism of LUCAT1 in NSCLC cisplatin resistance.
Main Methods:
- Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR) to measure LUCAT1 expression.
- Cell Counting Kit-8 (CCK-8) assay and flow cytometry to assess cell viability and apoptosis.
- Mechanism assays to elucidate the regulatory pathways involved.
Main Results:
- LUCAT1 expression was significantly higher in cisplatin-resistant NSCLC cells (A549/DDP) compared to sensitive cells (A549).
- Overexpression of LUCAT1 enhanced cisplatin resistance, inhibited cell apoptosis, and altered cell cycle distribution in NSCLC cells.
- LUCAT1 overexpression led to increased Insulin-like Growth Factor 2 (IGF-2) expression.
Conclusions:
- LUCAT1 promotes cisplatin resistance in NSCLC by regulating cell cycle and apoptosis.
- LUCAT1 targets IGF-2, contributing to its role in chemoresistance.
- LUCAT1 represents a potential therapeutic target for overcoming cisplatin resistance in NSCLC.
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