ArticleOncogene2016
Negative regulation of RNA-binding protein HuR by tumor-suppressor ECRG2.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- HuB serves as the central hub for connecting HuR-related mRNAs with translation machinery in inflammation.Communications biology · 2025Article
- The antiprotease Spink7 promotes inflammation resolution by modulating multiple proteases activities during wound healing.Clinical and translational medicine · 2025Article
- ECRG2/SPINK7 Tumor Suppressor as Modulator of DNA Damage Response.International journal of molecular sciences · 2024Review
- HuR as a molecular target for cancer therapeutics and immune-related disorders.Advanced drug delivery reviews · 2022Review
- Hu Antigen R (HuR) Protein Structure, Function and Regulation in Hepatobiliary Tumors.Cancers · 2022Review
- Cell-Penetrating Peptide TAT-HuR-HNS3 Suppresses Proinflammatory Gene Expression via Competitively Blocking Interaction of HuR with Its Partners.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The RNA-binding protein HuR in human cancer: A friend or foe?Advanced drug delivery reviews · 2022Review
- The versatile role of HuR in Glioblastoma and its potential as a therapeutic target for a multi-pronged attack.Advanced drug delivery reviews · 2022Review
- Roles of Embryonic Lethal Abnormal Vision-Like RNA Binding Proteins in Cancer and Beyond.Frontiers in cell and developmental biology · 2022Review
- LncRNA SNHG12 in extracellular vesicles derived from carcinoma-associated fibroblasts promotes cisplatin resistance in non-small cell lung cancer cells.Bioengineered · 2022Article
- Poly(ADP-ribosyl)ation enhances HuR oligomerization and contributes to pro-inflammatory gene mRNA stabilization.Cellular and molecular life sciences : CMLS · 2021Article
- Post-translational Control of RNA-Binding Proteins and Disease-Related Dysregulation.Frontiers in molecular biosciences · 2021Review
- ECRG2, a novel transcriptional target of p53, modulates cancer cell sensitivity to DNA damage.Cell death & disease · 2020Article
- Novel insights into PARPs in gene expression: regulation of RNA metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- CHTM1 regulates cancer cell sensitivity to metabolic stress via p38-AIF1 pathway.Journal of experimental & clinical cancer research : CR · 2019Article
- Integrated Regulation of HuR by Translation Repression and Protein Degradation Determines Pulsatile Expression of p53 Under DNA Damage.iScience · 2019Article
- RNA Binding Protein HuR Promotes Autophagosome Formation by Regulating Expression of Autophagy-Related Proteins 5, 12, and 16 in Human Hepatocellular Carcinoma Cells.Molecular and cellular biology · 2019Article
- The antiprotease SPINK7 serves as an inhibitory checkpoint for esophageal epithelial inflammatory responses.Science translational medicine · 2018Article
- α4 Coordinates Small Intestinal Epithelium Homeostasis by Regulating Stability of HuR.Molecular and cellular biology · 2018Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal cancer-related gene 2 (ECRG2) is a newer tumor suppressor whose function in the regulation of cell growth and apoptosis remains to be elucidated. Here we show that ECRG2 expression was upregulated in response to DNA damage, and increased ECRG2 expression induced growth suppression in cancer cells but not in non-cancerous epithelial cells. ECRG2-mediated growth suppression was associated with activation of caspases and marked reduction in the levels of apoptosis inhibitor, X chromosome-linked inhibitor of apoptosis protein (XIAP). ECRG2, via RNA-binding protein human antigen R (HuR), regulated XIAP mRNA stability and expression. Furthermore, ECRG2 increased HuR ubiquitination and degradation but was unable to modulate the non-ubiquitinable mutant form of HuR. We also identified missense and frame-shift ECRG2 mutations in various human malignancies and noted that, unlike wild-type ECRG2, one cancer-derived ECRG2 mutant harboring glutamic acid instead of valine at position 30 (V30E) failed to induce cell death and activation of caspases. This naturally occurring V30E mutant also did not suppress XIAP and HuR. Importantly, the V30E mutant overexpressing cancer cells acquired resistance against multiple anticancer drugs, thus suggesting that ECRG2 mutations appear to have an important role in the acquisition of anticancer drug resistance in a subset of human malignancies.
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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.