ArticleAging2016
ERP44 inhibits human lung cancer cell migration mainly via IP3R2.
Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Organelle contact sites in cancer cells.Cell death & disease · 2026Review
- Prognostic significance and therapeutic implications of redox metabolism-related genes in head and neck squamous cell carcinoma.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- ERp44 Regulates the Proliferation, Migration, Invasion, and Apoptosis of Gastric Cancer Cells Via Activation of ER Stress.Biochemical genetics · 2023Article
- PD-L1/p-STAT3 promotes the progression of NSCLC cells by regulating TAM polarization.Journal of cellular and molecular medicine · 2022Article
- Platelet-Derived Extracellular Vesicles Stimulate Migration through Partial Remodelling of the CaCells · 2022Article
- ERp44 is required for endocardial cushion development by regulating VEGFA secretion in myocardium.Cell proliferation · 2022Article
- Citrin mediated metabolic rewiring in response to altered basal subcellular CaCommunications biology · 2022Article
- Systematic Analysis of Molecular Subtypes and Immune Prediction Based on CD8 T Cell Pattern Genes Based on Head and Neck Cancer.Journal of oncology · 2022Article
- Cytotoxic capability and the associated proteomic profile of cell-free coelomic fluid extracts from the edible sea cucumberEXCLI journal · 2022Article
- Advances in Intracellular Calcium Signaling Reveal Untapped Targets for Cancer Therapy.Biomedicines · 2021Review
- ER resident protein 44 promotes malignant phenotype in nasopharyngeal carcinoma through the interaction with ATP citrate lyase.Journal of translational medicine · 2021Article
- Deciphering the Role of CaCancers · 2021Review
- FUNDC1 interacts with FBXL2 to govern mitochondrial integrity and cardiac function through an IP3R3-dependent manner in obesity.Science advances · 2020Article
- Lessons from the Endoplasmic Reticulum CaCells · 2020Review
- Impact of 17β-HSD12, the 3-ketoacyl-CoA reductase of long-chain fatty acid synthesis, on breast cancer cell proliferation and migration.Cellular and molecular life sciences : CMLS · 2020Article
- Article
- ERP44 Is Associated With Poor Prognosis and Promotes Proliferation and Temozolomide Resistance in Lower-grade Glioma.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cell migration is involved in tumour metastasis. However, the relationship between calcium signalling and cancer migration is not well elucidated. In this study, we used the human lung adenocarcinoma A549 cell line to examine the role of endoplasmic reticulum protein 44 (ERP44), which has been reported to regulate calcium release inside of the endoplasmic reticulum (ER), in cell migration. We found that the inositol 1,4,5-trisphosphate receptors (IP3Rs/ITPRs) inhibitor 2-APB significantly inhibited A549 cell migration by inhibiting cell polarization and pseudopodium protrusion, which suggests that Ca2+ is necessary for A549 cell migration. Similarly, the overexpression of ERP44 reduced intracellular Ca2+ release via IP3Rs, altered cell morphology and significantly inhibited the migration of A549 cells. These phenomena were primarily dependent on IP3R2 because wound healing in A549 cells with IP3R2 rather than IP3R1 or IP3R3 siRNA was markedly inhibited. Moreover, the overexpression of ERP44 did not affect the migration of the human neuroblastoma cell line SH-SY5Y, which mainly expresses IP3R1. Based on the above observations, we conclude that ERP44 regulates A549 cell migration mainly via an IP3R2-dependent pathway.
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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.