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Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing
Published on: October 10, 2025
LncRNA CASC11 promotes the development of lung cancer through targeting microRNA-302/CDK1 axis
1Department of Thoracic Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, China. tianci2010@vip.qq.com.
Objective:
To elucidate whether long non-coding RNA cancer susceptibility candidate 11 (lncRNA CASC11) could participate in the development of lung cancer through targeting microRNA-302/CDK1 axis.
Patients And Methods:
Expression levels of CASC11, microRNA-302 and CDK1 in lung cancer tissues and paracancerous tissues were determined by quantitative real-time polymerase chain reaction (qRT-PCR). CASC11 expression in lung cancer cell lines was also determined. The regulatory effect of CASC11 on proliferative potential of lung cancer cells was accessed by cell counting kit-8 (CCK-8) and colony formation assay. The binding condition between microRNA-302 to CASC11 and CDK1 was evaluated by dual-luciferase reporter gene assay. CDK1 expression in lung cancer cells with CASC11 or microRNA-302 knockdown was detected by Western blot. The proliferation of lung cancer cells was determined after transfection of microRNA-302 inhibitor or co-transfection of microRNA-302 inhibitor and si-CASC11.
Results:
CASC11 and CDK1 were highly expressed, whereas microRNA-302 was lowly expressed in lung cancer tissues. Identically, CASC11 was highly expressed in lung cancer cell lines (A547, H157 and SPC-A-1) than controls as well. CASC11 knockdown attenuated proliferative capacity of lung cancer cells. The opposite trend was observed by microRNA-302 knockdown. Dual-luciferase reporter gene assay verified that CASC11 could bind to microRNA-302 and microRNA-302 could bind to CDK1. CDK1 expression in lung cancer cells was negatively regulated by CASC11. MicroRNA-302 knockdown reversed the inhibitory effect of CASC11 on CDK1 expression. The proliferation of lung cancer cells co-transfected with microRNA-302 inhibitor and si-CASC11 decreased compared with those transfected with microRNA-302 inhibitor.
Conclusions:
High expression of CASC11 promotes the development of lung cancer through upregulating CDK1 expression by binding to microRNA-302.
Insights
High expression of long non-coding RNA CASC11 promotes lung cancer by increasing CDK1 levels via microRNA-302. This study reveals a novel mechanism in lung cancer development.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Lung cancer is a leading cause of cancer-related mortality worldwide.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
- The specific role of lncRNA CASC11 in lung cancer pathogenesis remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of lncRNA CASC11 in lung cancer development.
- To determine if CASC11 targets the microRNA-302/CDK1 axis in lung cancer.
- To elucidate the underlying molecular mechanisms of CASC11 in lung cancer progression.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) to measure expression levels of CASC11, microRNA-302, and CDK1.
- Cell counting kit-8 (CCK-8) and colony formation assays to assess cell proliferation.
- Dual-luciferase reporter gene assay to confirm binding interactions between CASC11, microRNA-302, and CDK1.
- Western blot analysis to detect protein expression levels.
Main Results:
- lncRNA CASC11 and CDK1 were significantly upregulated, while microRNA-302 was downregulated in lung cancer tissues and cell lines.
- CASC11 knockdown inhibited lung cancer cell proliferation, whereas microRNA-302 knockdown promoted it.
- Dual-luciferase assays confirmed that CASC11 directly binds to microRNA-302, and microRNA-302 directly binds to CDK1.
- CASC11 promotes lung cancer cell proliferation by upregulating CDK1 expression through sponging microRNA-302.
Conclusions:
- lncRNA CASC11 plays a crucial role in promoting lung cancer development.
- The CASC11/microRNA-302/CDK1 axis represents a potential therapeutic target for lung cancer.
- Understanding this regulatory pathway provides insights into the molecular mechanisms of lung cancer.
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