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LY6K is a novel molecular target in bladder cancer on basis of integrate genome-wide profiling
R Matsuda1, H Enokida, T Chiyomaru
1Department of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan.
Background:
The aim of this study is to find a novel molecular target based on chromosomal alteration and array-based gene expression analyses in bladder cancer (BC). We investigated a cancer testis antigen, LY6K, which is located on chromosome 8q24.3.
Methods:
Five BC cell lines were subjected to high-resolution array-comparative genomic hybridisation with 244 000 probes. The expression levels of LY6K mRNA were evaluated in BC cell lines and clinical BC specimens by real-time reverse transcription-PCR. The cell lines were subjected to fluorescence in situ hybridisation of LY6K. Cell viability was evaluated by cell growth, wound healing, and matrigel invasion assays.
Results:
Typical gained loci (P<0.0001) at 6p21.33-p21.32, 8q24.3, 9q34.13, 11q13.1-q14.1, 12q13.12-q13.13, 16p13.3, and 20q11.21-q13.33 were observed in all of the cell lines. We focused on 8q24.3 locus where LY6K gene harbours, and it was the top upregulated one in the gene profile from the BC cell line. LY6K mRNA expression was significantly higher in 91 BCs than in 37 normal bladder epitheliums (P<0.0001). Fluorescence in situ hybridisation validated that the high LY6K mRNA expression was due to gene amplification in the region where the gene harbours. Cell viability assays demonstrated that significant inhibitions of cell growth, migration, and invasion occured in LY6K knock down BC cell lines; converse phenomena were observed in a stable LY6K transfectant; and LY6K knockdown of the transfectant retrieved the original phenotype from the LY6K transfectant.
Conclusion:
Upregulation of the oncogenic LY6K gene located on the gained locus at 8q24.3 may contribute BC development.
Insights
The oncogenic LY6K gene, amplified on chromosome 8q24.3, is significantly upregulated in bladder cancer (BC). Its increased expression drives BC cell growth, migration, and invasion, suggesting LY6K as a potential therapeutic target.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Bladder cancer (BC) research seeks novel molecular targets.
- Chromosomal alterations and gene expression analyses are key to identifying these targets.
- The cancer testis antigen LY6K, located on chromosome 8q24.3, was investigated.
Purpose of the Study:
- To identify a novel molecular target for bladder cancer.
- To investigate the role of the LY6K gene in BC development.
- To correlate chromosomal alterations with LY6K gene expression in BC.
Main Methods:
- High-resolution array-comparative genomic hybridization (aCGH) on five BC cell lines.
- Real-time reverse transcription-PCR to evaluate LY6K mRNA expression in cell lines and clinical specimens.
- Fluorescence in situ hybridization (FISH) to confirm gene amplification.
- Cell viability assays including growth, wound healing, and matrigel invasion.
Main Results:
- Consistent chromosomal gains observed across BC cell lines, notably at 8q24.3.
- LY6K gene on 8q24.3 was significantly upregulated and amplified in BC.
- Elevated LY6K mRNA expression in 91 BC samples compared to 37 normal bladder tissues.
- LY6K knockdown inhibited BC cell growth, migration, and invasion; LY6K overexpression promoted these processes.
Conclusions:
- The oncogenic LY6K gene, located on the amplified 8q24.3 locus, contributes to bladder cancer development.
- LY6K's role in promoting cell proliferation, migration, and invasion highlights its potential as a therapeutic target.
- Targeting LY6K may offer a novel strategy for bladder cancer treatment.
