ArticleBMC ophthalmology2020
Different transcriptome profiles between human retinoblastoma Y79 cells and an etoposide-resistant subline reveal a chemoresistance mechanism.
Article in BMC ophthalmology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 17 citations in OpenAlex.
- Effect of ARHGAP9 on Chemoresistance in High-Risk Advanced Retinoblastoma via the Rac1/β-Catenin/LEF1 Signaling Axis.Investigative ophthalmology & visual science · 2026Article
- Retinoblastoma and Its Tumor Microenvironment.Current oncology (Toronto, Ont.) · 2026Review
- Mimicking Retinoblastoma Treatment With Repeated Topotecan or Melphalan Develops Cross-Resistance to Classic Agents But Not to Repurposed Drugs.Investigative ophthalmology & visual science · 2024Article
- Comparative study on genomic and epigenomic profiles of retinoblastoma or tuberous sclerosis complex via nanopore sequencing and a joint screening framework.Cancer gene therapy · 2024Article
- Identifying Treatment Resistance Related Pathways by Analyzing Serum Extracellular Vesicles of Patients With Resistant Versus Regressed Retinoblastoma.Investigative ophthalmology & visual science · 2023Article
- Retinoblastoma: A review of the molecular basis of tumor development and its clinical correlation in shaping future targeted treatment strategies.Indian journal of ophthalmology · 2023Review
- Long non-coding RNAs involved in retinoblastoma.Journal of cancer research and clinical oncology · 2023Review
- Downregulation of miR-211-5p Promotes Carboplatin Resistance in Human Retinoblastoma Y79 Cells by Affecting the GDNF-LIF Interaction.Frontiers in oncology · 2022Article
- RING-Finger Protein 6 promotes Drug Resistance in RetinoblastomaPathology oncology research : POR · 2022Article
- Review
- Long Noncoding RNA MALAT1 Promotes the Development of Colon Cancer by RegulatingOncoTargets and therapy · 2020Article
- Knockdown of lncRNA HOTTIP Inhibits Retinoblastoma Progression by Modulating the miR-101-3p/STC1 Axis.Technology in cancer research & treatmentArticle
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundRetinoblastoma (RB) is the most frequent pediatric retinal tumor. In the present study, to elucidate chemoresistance mechanisms and identify potential biomarkers in RB, we utilized RNA sequencing (RNAseq) technological platforms to reveal transcriptome profiles and identify any differentially expressed genes (DEGs) between an etoposide drug-resistant subline (Y79/EDR) and parental Y79 cells.
methodsTo test whether Y79/EDR cells showed resistance to antineoplastic agents for RB, we treated the cells with etoposide, carboplatin and vincristine and analyzed them with a Cell Counting Kit-8 (CCK-8). Y79/EDR and parental Y79 cells were used for RNAseq and bioinformatics analysis to enable a genome-wide review of DEGs between the two lines using the DESeq R package (1.10.1). Then, DEG enrichment in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways was analyzed with KOBAS software. Next, real-time quantitative reverse transcription polymerase chain reaction (real time QRT-PCR) and cytotoxicity assays were performed to experimentally and functionally validate the identified candidate biomarkers.
resultsY79/EDR cells showed resistance to etoposide, carboplatin and vincristine at different concentrations. In total, 524 transcripts were differentially expressed in Y79/EDR cells based on analysis of fragments per kilobase of transcript per million fragments mapped (FPKM); among these, 57 genes were downregulated and 467 genes were upregulated in Y79/EDR cells compared to parental Y79 cells. We selected candidate DEGs, including ARHGAP9, HIST1H4H, RELN, DDIT4, HK2, STC1 and PFKFB4, for mRNA expression validation with real time QRT-PCR assays and found that the expression levels determined by real time QRT-PCR were consistent with the RNAseq data. Further studies involving downregulation of ARHGAP9 with a specific siRNA showed that ARHGAP9 altered the cellular sensitivity of Y79 cells to etoposide and carboplatin.
conclusionOur initial findings provided a genomic view of the transcription profiles of etoposide-induced acquired resistance in RB. Follow-up studies indicated that ARHGAP9 might be a chemoresistance biomarker in RB, providing insight into potential therapeutic targets for overcoming acquired chemoresistance in RB. These findings can aid in understanding and overcoming chemoresistance during treatment of RB in the clinic.
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