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Updated: Jan 23, 2026

Endobronchial Ultrasound-guided Intratumoral Injection of Cisplatin for the Treatment of Isolated Mediastinal Recurrence of Lung Cancer
Published on: February 12, 2017
Long noncoding RNA OR3A4 promotes cisplatin resistance of non-small cell lung cancer by upregulating CDK1
1Department of Central Sterile Supply, Yantai Yuhuangding Hospital, Yantai, China. YSLM0142@outlook.com.
Objective:
Numerous studies have proved that long non-coding RNAs (lncRNAs) have an important role in malignant tumors, including non-small cell lung cancer (NSCLC). LncRNA olfactory receptor family 3 subfamily A member 4 (OR3A4) was explored to identify how it functions in resistance of NSCLC patients to cisplatin.
Materials And Methods:
Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect OR3A4 expression in NSCLC patients. Then, we conducted Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis to detect the function of OR3A4 on the resistance of NSCLC cells to cisplatin. Furthermore, the potential mechanism was explored by mechanism assays.
Results:
Compared with OR3A4 expression of paired A549 cells, OR3A4 expression of A549/DDP cells was higher. Moreover, the functional assay showed that after OR3A4 was silenced in A549/DDP cells, cell cycle arrest and cell apoptosis was induced, and resistance to cisplatin was reversed. Furthermore, it was found that CDK1 expression was suppressed in A549/DDP cells by knockdown of OR3A4.
Conclusions:
The present work suggests that OR3A4 participates in regulating cell cycle, cell apoptosis of NSCLC cells and the resistance to cisplatin via upregulating CDK1, indicating that OR3A4 could be identified as a potential therapeutic target for NSCLC patients.
Insights
Long non-coding RNA OR3A4 promotes cisplatin resistance in non-small cell lung cancer (NSCLC) by upregulating CDK1. Silencing OR3A4 reverses resistance, offering a potential therapeutic target for NSCLC patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) play a critical role in various cancers, including non-small cell lung cancer (NSCLC).
- Understanding the specific functions of lncRNAs in drug resistance is crucial for developing effective cancer therapies.
Purpose of the Study:
- To investigate the role of lncRNA olfactory receptor family 3 subfamily A member 4 (OR3A4) in cisplatin resistance in NSCLC.
- To explore the underlying molecular mechanisms by which OR3A4 influences cisplatin sensitivity.
Main Methods:
- Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to measure OR3A4 expression levels.
- Cell Counting Kit-8 (CCK-8) and flow cytometry were employed to assess the functional impact of OR3A4 on NSCLC cell viability and apoptosis.
- Mechanism assays were performed to elucidate the molecular pathways involved.
Main Results:
- OR3A4 expression was significantly higher in cisplatin-resistant NSCLC cells (A549/DDP) compared to sensitive cells (A549).
- Silencing OR3A4 in A549/DDP cells induced cell cycle arrest and apoptosis, and reversed cisplatin resistance.
- Knockdown of OR3A4 led to the suppression of CDK1 expression in resistant NSCLC cells.
Conclusions:
- OR3A4 promotes cisplatin resistance in NSCLC by upregulating CDK1, affecting cell cycle and apoptosis.
- OR3A4 represents a potential therapeutic target for overcoming cisplatin resistance in non-small cell lung cancer patients.
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