ArticleJournal of the National Cancer Institute2013
Unraveling the role of KIAA1199, a novel endoplasmic reticulum protein, in cancer cell migration.
Article in Journal of the National Cancer Institute, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
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Who cites it
84 citing papers in PubMed, 143 citations in OpenAlex.
- NSUN2/ALYREF-mediated RNA m5c modification promotes anoikis resistance of prostate cancer through activating autophagy.Oncogene · 2026Article
- CEMIP promotes gefitinib resistance in lung cancer with EGFR-mutation possibly through forming a stable complex CEMIP/c-MYC.BBA advances · 2026Article
- HSPA5, a Host Cellular Heat-Shock Protein Required for Influenza a Virus Replication.International journal of molecular sciences · 2025Article
- CEMIP Maintains Vascular Contractility by Controlling PP1c-MLC20 Cascade in SMCs.Circulation research · 2025Article
- Evaluation of CEMIP in diagnosis of pancreatic carcinoma in comparison with other traditional markers.Scientific reports · 2025Article
- Extracellular vesicles: the "Trojan Horse" within breast cancer host microenvironments.Molecular cancer · 2025Review
- Hyaluronan-Binding Protein Promotes Fibroblast Transformation and Heart Failure by Modulating the STAT5A-MMP13 Pathway.Biomedicines · 2025Article
- Targeting pyroptosis reverses KIAA1199-mediated immunotherapy resistance in colorectal cancer.Journal for immunotherapy of cancer · 2025Article
- The crucial role of CEMIP in cancer metastasis: Mechanistic insights and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- New molecules indispensable for hyaluronan degradation, HYBID (CEMIP/KIAA1199) and TMEM2 (CEMIP2): Differential roles in physiological and pathological non-neoplastic conditions.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025Review
- Genetic Deficiencies of Hyaluronan Degradation.Cells · 2024Review
- CCDC88C, an O-GalNAc glycosylation substrate of GALNT6, drives breast cancer metastasis by promoting c-JUN-mediated CEMIP transcription.Cancer cell international · 2024Article
- Identification of a Novel Mesenchymal Stem Cell-Related Signature for Predicting the Prognosis and Therapeutic Responses of Bladder Cancer.Stem cells international · 2024Article
- The novel epithelial-mesenchymal transition-related proteins and their therapeutic targets in cholangiocarcinoma: a narrative review.Journal of gastrointestinal oncology · 2023Review
- HIF1α/CCL7/KIAA1199 axis mediates hypoxia-induced gastric cancer aggravation and glycolysis alteration.Journal of clinical biochemistry and nutrition · 2023Article
- KIAA1199 deficiency enhances skeletal stem cell differentiation to osteoblasts and promotes bone regeneration.Nature communications · 2023Article
- Effects of Selenium Yeast on Egg Quality, Plasma Antioxidants, Selenium Deposition and Eggshell Formation in Aged Laying Hens.Animals : an open access journal from MDPI · 2023Article
- CEMIP, acting as a scaffold protein for bridging GRAF1 and MIB1, promotes colorectal cancer metastasis via activating CDC42/MAPK pathway.Cell death & disease · 2023Article
- Molecular mechanisms of microRNA-216a during tumor progression.Cancer cell international · 2023Review
- Rat Mammary carcinoma susceptibility 3 (Mcs3) pleiotropy, socioenvironmental interaction, and comparative genomics with orthologous human 15q25.1-25.2.G3 (Bethesda, Md.) · 2023Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCell migration is a critical determinant of cancer metastasis, and a better understanding of the genes involved will lead to the identification of novel targets aimed at preventing cancer dissemination. KIAA1199 has been shown to be upregulated in human cancers, yet its role in cancer progression was hitherto unknown.
methodsClinical relevance was assessed by examining KIAA1199 expression in human cancer specimens. In vitro and in vivo studies were employed to determine the function of KIAA1199 in cancer progression. Cellular localization of KIAA1199 was microscopically determined. SNAP-tag pull-down assays were used to identify binding partner(s) of KIAA1199. Calcium levels were evaluated using spectrofluorometric and fluorescence resonance energy transfer analyses. Signaling pathways were dissected by Western blotting. Student t test was used to assess differences. All statistical tests were two-sided.
resultsKIAA1199 was upregulated in invasive breast cancer specimens and inversely associated with patient survival rate. Silencing of KIAA1199 in MDA-MB-435 cancer cells resulted in a mesenchymal-to-epithelial transition that reduced cell migratory ability in vitro (75% reduction; P < .001) and decreased metastasis in vivo (80% reduction; P < .001). Gain-of-function assays further demonstrated the role of KIAA1199 in cell migration. KIAA1199-enhanced cell migration required endoplasmic reticulum (ER) localization, where it forms a stable complex with the chaperone binding immunoglobulin protein (BiP). A novel ER-retention motif within KIAA1199 that is required for its ER localization, BiP interaction, and enhanced cell migration was identified. Mechanistically, KIAA1199 was found to mediate ER calcium leakage, and the resultant increase in cytosolic calcium ultimately led to protein kinase C alpha activation and cell migration.
conclusionsKIAA1199 serves as a novel cell migration-promoting gene and plays a critical role in maintaining cancer mesenchymal status.
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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.