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Updated: Aug 1, 2025
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
microRNA-660 Enhances Cisplatin Sensitivity via Decreasing SATB2 Expression in Lung Adenocarcinoma
Ziyao Wang1, Lingxuan Zhou1, Bisong Chen2
1Department of Thoracic Surgery, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University/Hunan Cancer Hospital, Changsha 410006, China.
Abstract:
Increasing evidence suggests that microRNAs' (miRNAs) abnormal expression is one of the main factors of chemotherapy resistance in various cancers. However, the role of miRNAs in lung adenocarcinoma (LUAD) resistance to cisplatin is still unclear. In this study, we analyzed a microarray dataset to investigate miRNAs related to cisplatin resistance in LUAD. The expression of miRNAs in LUAD tissues and cell lines was detected using real-time quantitative polymerase chain reaction (RT-qPCR). Special AT-Rich Sequence-Binding Protein 2 (SATB2) in LUAD cell lines was detected using RT-qPCR and Western blot. Cell proliferation was measured by CCK8 and colony formation assays, while cell cycle and apoptosis were measured by flow cytometry. A dual-luciferase reporter assay was performed to confirm that SATB2 is a target gene of microRNA-660 (miR-660). We showed that the expression of miR-660 was not only decreased in LUAD cells and tissues but also further decreased in the cisplatin-resistant A549 cell line. The overexpression of miR-660 increased cisplatin sensitivity in LUAD cells. In addition, we identified SATB2 as a direct target gene of miR-660. We also revealed that miR-660 increased cisplatin sensitivity in LUAD cells via targeting SATB2. In conclusion, miR-660/SATB2 axis is a key regulator of cisplatin resistance in LUAD.
Insights
MicroRNA-660 (miR-660) is downregulated in lung adenocarcinoma (LUAD) and its restoration enhances cisplatin sensitivity. The miR-660/SATB2 axis regulates cisplatin resistance in LUAD.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Chemotherapy resistance is a major challenge in cancer treatment.
- MicroRNAs (miRNAs) are implicated in various cancers' resistance mechanisms.
- The specific role of miRNAs in lung adenocarcinoma (LUAD) cisplatin resistance remains largely unknown.
Purpose of the Study:
- To investigate the role of miRNAs in LUAD cisplatin resistance.
- To identify specific miRNAs and their targets involved in this process.
- To elucidate the regulatory mechanism of cisplatin resistance in LUAD.
Main Methods:
- Analysis of microarray datasets for miRNA expression.
- Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot for gene expression analysis.
- Cell proliferation, cell cycle, and apoptosis assays (CCK8, colony formation, flow cytometry).
- Dual-luciferase reporter assay to confirm miRNA-target interaction.
Main Results:
- MicroRNA-660 (miR-660) expression was decreased in LUAD tissues and cells, with further reduction in cisplatin-resistant cells.
- Overexpression of miR-660 enhanced LUAD cells' sensitivity to cisplatin.
- Special AT-Rich Sequence-Binding Protein 2 (SATB2) was identified as a direct target gene of miR-660.
- miR-660 increased cisplatin sensitivity by targeting SATB2.
Conclusions:
- The miR-660/SATB2 axis plays a crucial role in regulating cisplatin resistance in LUAD.
- miR-660 functions as a tumor suppressor by enhancing chemosensitivity.
- Targeting the miR-660/SATB2 pathway may offer a novel therapeutic strategy for LUAD.
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