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MiR-320a is associated with cisplatin resistance in lung adenocarcinoma and its clinical value in non-small cell lung
Min Lu1, Chunhong Hu1, Fang Wu2
1Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Background:
Currently, the main treatment for non-small cell lung cancer (NSCLC) is surgery and chemotherapy. Although major progress has been made in targeted treatment and immunotherapy, the survival rates for this disease are still low and associated with resistance to chemotherapy. Previous studies have shown that histone acetylation and microRNAs (miRNAs) might play an important role in chemotherapy resistance. The aim of this study was to identify candidate miRNAs related to cisplatin (DDP) resistance in lung adenocarcinoma.
Methods:
We used 5-aza-2'-deoxycytidine and trichostatin A to reverse the drug resistance of A549/DDP cells in vitro, and miRNA expression profiling was performed by microarrays to identify candidate miRNAs. In addition, we investigated the correlations between miR-320a expression and clinical characteristics through data collected from Gene Expression Omnibus (GEO) microarrays, and The Cancer Genome Atlas (TCGA) to determine the clinical role of miR-320a in lung adenocarcinoma. Furthermore, we investigated the biological function of miR-320a. TargetScanHuman, PicTar2005 and miRanda v5.1. were used to predict the target genes of miR-320a; then, the function of these genes were suggested from the enrichment of GO categories items and KEGG analyses.
Results:
Treatment with 5-Aza-dc significantly inhibited cellular proliferation, and increased apoptosis in the A549/DDP cells compared with the untreated cells. TSA did not reverse cisplatin resistance. MiR-320a was up-regulated during reversal of cisplatin resistance. The lung adenocarcinoma groups had a significantly lower level of miR-320a expression than the control groups. For the bioinformatics analyses, we found some target genes involved in cell cycle progression, tumor progression, the MAPK signaling pathway, and the ErbB signaling pathway. The promising target genes were highly enriched in various pathways in cancer.
Conclusions:
The current study confirmed miR-320a was up-regulated during the revering of cisplatin resistance. The results of bioinformatics analyses may present a new method for investigating the pathogenesis of lung adenocarcinoma.
Insights
This study found that miR-320a is upregulated when cisplatin resistance is reversed in lung adenocarcinoma. Lower miR-320a levels correlate with lung adenocarcinoma, suggesting its role in chemotherapy resistance.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-small cell lung cancer (NSCLC) treatments like surgery and chemotherapy have limited efficacy due to drug resistance.
- MicroRNAs (miRNAs) and histone acetylation are implicated in chemotherapy resistance.
- Identifying miRNAs associated with cisplatin resistance is crucial for improving lung adenocarcinoma treatment.
Purpose of the Study:
- To identify candidate miRNAs involved in cisplatin (DDP) resistance in lung adenocarcinoma.
- To investigate the clinical role and biological function of miR-320a in lung adenocarcinoma.
Main Methods:
- Drug resistance reversal in A549/DDP cells using 5-aza-2'-deoxycytidine and trichostatin A.
- miRNA expression profiling via microarrays.
- Bioinformatic analyses of miR-320a expression in lung adenocarcinoma using GEO and TCGA datasets.
- Prediction of miR-320a target genes and functional enrichment analysis (GO, KEGG).
Main Results:
- 5-Aza-dc treatment inhibited proliferation and increased apoptosis in A549/DDP cells; TSA did not reverse cisplatin resistance.
- miR-320a was significantly upregulated during the reversal of cisplatin resistance.
- Lung adenocarcinoma patients exhibited lower miR-320a expression compared to controls.
- Bioinformatic analysis identified miR-320a targets involved in cell cycle, tumor progression, MAPK, and ErbB signaling pathways.
Conclusions:
- miR-320a upregulation is confirmed during the reversal of cisplatin resistance in lung adenocarcinoma.
- The identified miR-320a targets and pathways offer potential insights into lung adenocarcinoma pathogenesis and therapeutic strategies.
