ArticleThe Journal of biological chemistry2013
Epidermal growth factor promotes protein degradation of epithelial protein lost in neoplasm (EPLIN), a putative metastasis suppressor, during epithelial-mesenchymal transition.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 45 citations in OpenAlex.
- EPLIN stabilizes cell-cell adhesion complexes to facilitate TGF-β1-induced fibroblastic differentiation of human periodontal ligament stem cells.Stem cells (Dayton, Ohio) · 2026Article
- CDK1-mediated phosphorylation of EPLIN is crucial for mitotic spindle positioning.Communications biology · 2026Article
- Bisphosphate nucleotidase 1 promotes progression and docetaxel resistance in triple-negative breast cancer via STUB1-mediated destabilization of LIMA1.Cell death & disease · 2026Article
- Integrative multi-omics analysis implicates the RNF40-LIMA1 axis in hepatocellular carcinoma progression and immune microenvironment remodeling.Frontiers in oncology · 2026Article
- The isobaric tags for relative and absolute quantification-based quantitative proteomics of fresh tissue-derived secretome in hepatocellular carcinoma.Archives of medical science : AMS · 2025Article
- EPLIN, a prospective oncogenic molecule with contribution to growth, migration and drug resistance in pancreatic cancer.Scientific reports · 2024Article
- Expression and molecular insights of lima1 in cholangiocarcinoma.Cell adhesion & migration · 2024Article
- LIMA1 links the E3 ubiquitin ligase RNF40 to lipid metabolism.Cell death discovery · 2024Article
- Exploring the Enigma: The Role of the Epithelial Protein Lost in Neoplasm in Normal Physiology and Cancer Pathogenesis.International journal of molecular sciences · 2024Review
- MAD2 activates IGF1R/PI3K/AKT pathway and promotes cholangiocarcinoma progression by interfering USP44/LIMA1 complex.Oncogene · 2023Article
- Nicardipine is a putative EED inhibitor and has high selectivity and potency against chemoresistant prostate cancer in preclinical models.British journal of cancer · 2023Article
- Characterization of LIMA1 and its emerging roles and potential therapeutic prospects in cancers.Frontiers in oncology · 2023Review
- EPLIN, a Putative Tumour Suppressor in Colorectal Cancer, Implications in Drug Resistance.International journal of molecular sciences · 2022Article
- Epithelial Protein Lost in Neoplasm, EPLIN, the Cellular and Molecular Prospects in Cancers.Biomolecules · 2021Review
- Rab40-Cullin5 complex regulates EPLIN and actin cytoskeleton dynamics during cell migration.The Journal of cell biology · 2021Article
- Article
- Phenotypic Plasticity of Cancer Cells Based on Remodeling of the Actin Cytoskeleton and Adhesive Structures.International journal of molecular sciences · 2021Review
- Epithelial protein lost in neoplasm (EPLIN) and prostate cancer: lessons learned from the ARCaP model.American journal of clinical and experimental urology · 2021Review
- Pharmacological inhibition of noncanonical EED-EZH2 signaling overcomes chemoresistance in prostate cancer.Theranostics · 2021Article
- Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Aberrant expression of EGF receptors has been associated with hormone-refractory and metastatic prostate cancer (PCa). However, the molecular mechanism for EGF signaling in promoting PCa metastasis remains elusive. Using experimental models of PCa metastasis, we demonstrated that EGF could induce robust epithelial-mesenchymal transition (EMT) and increase invasiveness. Interestingly, EGF was found to be capable of promoting protein turnover of epithelial protein lost in neoplasm (EPLIN), a putative suppressor of EMT and tumor metastasis. Mechanistic study revealed that EGF could activate the phosphorylation, ubiquitination, and degradation of EPLIN through an extracellular signal-regulated kinase 1/2 (ERK1/2)-dependent signaling cascade. Pharmacological inhibition of the ERK1/2 pathway effectively antagonized EGF-induced EPLIN degradation. Two serine residues, i.e. serine 362 and serine 604, were identified as putative ERK1/2 phosphorylation sites in human EPLIN, whose point mutation rendered resistance to EGF-induced protein turnover. This study elucidated a novel molecular mechanism for EGF regulation of EMT and invasiveness in PCa cells, indicating that blockade of EGF signaling could be beneficial in preventing and retarding PCa metastasis at early stages.
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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.