ArticleProceedings of the National Academy of Sciences of the United States of America2012
Evolutionarily conserved protein ERH controls CENP-E mRNA splicing and is required for the survival of KRAS mutant cancer cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 72 citations in OpenAlex.
- Potential Mechanisms of MAP Kinase JNK's Involvement in Modulating Cancer Cell Fate in a Cisplatin Concentration-Dependent Manner.Pharmaceuticals (Basel, Switzerland) · 2026Article
- RSRC2 is a novel RNA-binding protein that safeguards mitotic fidelity by interacting with the lncRNA C1QTNF1-AS1.Nucleic acids research · 2026Article
- ERH promotes primary microRNA processing beyond cluster assistance.Nature communications · 2025Article
- ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA.Nucleic acids research · 2025Article
- ERH Impacts Patient Prognosis and Tumor Immune Microenvironment: A Pan-Cancer Analysis.Combinatorial chemistry & high throughput screening · 2025Article
- Upregulated enhancer of rudimentary homolog promotes epithelial‑mesenchymal transition and cancer cell migration in lung adenocarcinoma.Molecular medicine reports · 2024Article
- MYCN and SNRPD3 cooperate to maintain a balance of alternative splicing events that drives neuroblastoma progression.Oncogene · 2024Article
- CRISPR-mediated reversion of oncogenic KRAS mutation results in increased proliferation and reveals independent roles of Ras and mTORC2 in the migration of A549 lung cancer cells.Molecular biology of the cell · 2023Article
- Review
- ZNF330/NOA36 interacts with HSPA1 and HSPA8 and modulates cell cycle and proliferation in response to heat shock in HEK293 cells.Biology direct · 2023Article
- HPV16 E6 induces chromosomal instability due to polar chromosomes caused by E6AP-dependent degradation of the mitotic kinesin CENP-E.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Chemical acylation of an acquired serine suppresses oncogenic signaling of K-Ras(G12S).Nature chemical biology · 2022Article
- Review
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- ERH Gene and Its Role in Cancer Cells.Frontiers in oncology · 2022Review
- ERH Interacts With EIF2α and Regulates the EIF2α/ATF4/CHOP Pathway in Bladder Cancer Cells.Frontiers in oncology · 2022Article
- Non-targeting control for MISSION shRNA library silencesMolecular therapy. Nucleic acids · 2021Article
- Molecular basis for PICS-mediated piRNA biogenesis and cell division.Nature communications · 2021Article
- Apoptotic Effects of Anthocyanins fromInternational journal of molecular sciences · 2021Article
- ERH facilitates microRNA maturation through the interaction with the N-terminus of DGCR8.Nucleic acids research · 2020Article
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 2 countries.
Funding
Abstract
Cancers with Ras mutations represent a major therapeutic problem. Recent RNAi screens have uncovered multiple nononcogene addiction pathways that are necessary for the survival of Ras mutant cells. Here, we identify the evolutionarily conserved gene enhancer of rudimentary homolog (ERH), in which depletion causes greater toxicity in cancer cells with mutations in the small GTPase KRAS compared with KRAS WT cells. ERH interacts with the spliceosome protein SNRPD3 and is required for the mRNA splicing of the mitotic motor protein CENP-E. Loss of ERH leads to loss of CENP-E and consequently, chromosome congression defects. Gene expression profiling indicates that ERH is required for the expression of multiple cell cycle genes, and the gene expression signature resulting from ERH down-regulation inversely correlates with KRAS signatures. Clinically, tumor ERH expression is inversely associated with survival of colorectal cancer patients whose tumors harbor KRAS mutations. Together, these findings identify a role of ERH in mRNA splicing and mitosis, and they provide evidence that KRAS mutant cancer cells are dependent on ERH for their survival.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.