Related Experiment Video
Updated: Jun 26, 2025

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
Transposable elements alter gene expression and may impact response to cisplatin therapy in ovarian cancer
Daniela Moreira Mombach1, Rafael Luiz Vieira Mercuri2,3, Tiago Minuzzi Freire da Fontoura Gomes1
1Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Abstract:
Cisplatin is widely employed for cancer treatment; therefore, understanding resistance to this drug is critical for therapeutic practice. While studies have delved into differential gene expression in the context of cisplatin resistance, findings remain somewhat scant. We performed a comprehensive investigation of transposable elements (TEs) expression and their impact in host genes in two cisplatin-treated ovarian cancer cell lines. RNA-seq, ATAC-seq, and in-depth bioinformatics analysis were used to compare cisplatin-sensitive and -resistant ovarian cancer cell lines. Our results reveal that cisplatin therapy alters not only the expression of protein-coding genes, but also key TEs, including LINE1, Alu, and endogenous retroviruses, in both cisplatin-sensitive and -resistant cell lines. By co-expressing with downstream genes or by creating chimeric transcripts with host genes at their insertion sites, these TEs seem to control the expression of protein-coding genes, including tumor-related genes. Our model uncovers TEs influencing the expression of cancer genes and cancer pathways. Collectively, our findings indicate that TE alterations associated with cisplatin treatment occur in critical cancer genes and cellular pathways synergically. This research highlights the importance of considering the entire spectrum of transcribed elements in the genome, especially TE expression, for a complete understanding of complex models like cancer response to treatment.
Insights
Transposable elements (TEs) like LINE1 and Alu are altered by cisplatin treatment in ovarian cancer cells. These TEs influence cancer genes and pathways, impacting drug resistance.
Area of Science:
- Genomics
- Cancer Biology
- Molecular Oncology
Background:
- Cisplatin is a cornerstone chemotherapy drug, but understanding cancer's resistance mechanisms is crucial for improving patient outcomes.
- While gene expression changes are studied, the role of transposable elements (TEs) in cisplatin resistance remains underexplored.
Purpose of the Study:
- To comprehensively investigate the expression and functional impact of transposable elements (TEs) in cisplatin-resistant ovarian cancer.
- To elucidate how TEs influence host gene expression and cellular pathways in response to cisplatin therapy.
Main Methods:
- Utilized RNA-sequencing (RNA-seq) and ATAC-sequencing (ATAC-seq) to compare cisplatin-sensitive and -resistant ovarian cancer cell lines.
- Performed in-depth bioinformatics analysis to identify altered TEs and their interactions with host genes.
Main Results:
- Cisplatin treatment significantly altered the expression of key TEs (LINE1, Alu, endogenous retroviruses) in both sensitive and resistant cell lines.
- TEs were found to co-express with or form chimeric transcripts with host genes, potentially regulating tumor-related genes.
- A model was developed demonstrating TEs influencing cancer genes and pathways critical for cisplatin response.
Conclusions:
- Transposable element alterations are a significant consequence of cisplatin treatment, affecting critical cancer genes and pathways.
- Considering the full spectrum of genomic elements, particularly TEs, is essential for a complete understanding of cancer treatment response and resistance.
Related Concept Videos
Overview of Transposition and Recombination
DNA-only Transposons
The donor site from where the transposon is excised is either degraded or...
Non-LTR Retrotransposons
piRNA - Piwi-interacting RNAs
Induced Pluripotent Stem Cells
Somatic...
Treatment Resistant Cancers

