Long noncoding LUCAT1 promotes cisplatin resistance of non-small cell lung cancer by promoting IGF-2

W. Wang, M.-L. Dong, W. Zhang, T. Liu

Department of Pharmacy, Yantai Yuhuangding Hospital, Yantai, China. liutao567@163.com

---

• Oncology

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.

This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause.

Free PDF Download