ArticleNucleic acids research2020
ZRANB2 and SYF2-mediated splicing programs converging on ECT2 are involved in breast cancer cell resistance to doxorubicin.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
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- Nuclear activities and interactome of the NS5 protein of Tick-Borne Encephalitis Virus.bioRxiv : the preprint server for biology · 2026Article
- Splicing as an integrative layer linking cell cycle regulation, epigenetic dynamics, and environmental responses in plants.Frontiers in plant science · 2026Review
- Dual modes of contractility tailor cytokinesis to the requirements of diverse tissues.iScience · 2025Article
- Genome-wide selection signal analysis reveals copy number variation associated with litter size in Guizhou Black goat.Frontiers in veterinary science · 2025Article
- Identification of hub genes and pathways in Uterine corpus endometrial carcinoma (UCEC): A comprehensiveBiochemistry and biophysics reports · 2024Article
- Research progress on the relationship between AURKA and tumorigenesis: the neglected nuclear function of AURKA.Annals of medicine · 2024Review
- Systematic identification of interchromosomal interaction networks supports the existence of specialized RNA factories.Genome research · 2024Article
- Sex-related differences in delayed doxorubicin-induced cardiac dysfunction in C57BL/6 mice.Archives of toxicology · 2024Article
- Two RhoGEF isoforms with distinct localisation control furrow position during asymmetric cell division.Nature communications · 2023Article
- The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress.Nucleic acids research · 2022Article
- Alternative splicing of HSPA12A pre-RNA by SRSF11 contributes to metastasis potential of colorectal cancer.Clinical and translational medicine · 2022Article
- Glucocorticoids mediate transcriptome-wide alternative polyadenylation: Potential mechanistic and clinical implications.Clinical and translational science · 2022Article
- DNA Damage Regulates the Functions of the RNA Binding Protein Sam68 through ATM-Dependent Phosphorylation.Cancers · 2022Article
- Single-Cell RNA-Seq Analysis of Cells from Degenerating and Non-Degenerating Intervertebral Discs from the Same Individual Reveals New Biomarkers for Intervertebral Disc Degeneration.International journal of molecular sciences · 2022Article
- HLA-DQB1-AS1 Promotes Cell Proliferation, Inhibits Apoptosis, and Binds with ZRANB2 Protein in Hepatocellular Carcinoma.Journal of oncology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Besides analyses of specific alternative splicing (AS) variants, little is known about AS regulatory pathways and programs involved in anticancer drug resistance. Doxorubicin is widely used in breast cancer chemotherapy. Here, we identified 1723 AS events and 41 splicing factors regulated in a breast cancer cell model of acquired resistance to doxorubicin. An RNAi screen on splicing factors identified the little studied ZRANB2 and SYF2, whose depletion partially reversed doxorubicin resistance. By RNAi and RNA-seq in resistant cells, we found that the AS programs controlled by ZRANB2 and SYF2 were enriched in resistance-associated AS events, and converged on the ECT2 splice variant including exon 5 (ECT2-Ex5+). Both ZRANB2 and SYF2 were found associated with ECT2 pre-messenger RNA, and ECT2-Ex5+ isoform depletion reduced doxorubicin resistance. Following doxorubicin treatment, resistant cells accumulated in S phase, which partially depended on ZRANB2, SYF2 and the ECT2-Ex5+ isoform. Finally, doxorubicin combination with an oligonucleotide inhibiting ECT2-Ex5 inclusion reduced doxorubicin-resistant tumor growth in mouse xenografts, and high ECT2-Ex5 inclusion levels were associated with bad prognosis in breast cancer treated with chemotherapy. Altogether, our data identify AS programs controlled by ZRANB2 and SYF2 and converging on ECT2, that participate to breast cancer cell resistance to doxorubicin.
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