ArticleThe Journal of biological chemistry2010
Inositol 1,4,5-trisphosphate 3-kinase-A is a new cell motility-promoting protein that increases the metastatic potential of tumor cells by two functional activities.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- Structural insights into the development of inhibitors for inositol phosphate kinases.FEBS letters · 2026Review
- Evolutionarily conserved short linear motifs drive actin filament binding.Nature cell biology · 2026Article
- ITPKA promotes invasive phenotypes in clear cell renal cell carcinoma through functional modulation of PPAR signaling.American journal of cancer research · 2026Article
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- π-PrimeNovo: an accurate and efficient non-autoregressive deep learning model for de novo peptide sequencing.Nature communications · 2025Article
- Article
- Origin, evolution, and diversification of inositol 1,4,5-trisphosphate 3-kinases in plants and animals.BMC genomics · 2024Article
- Substrate promiscuity of inositol 1,4,5-trisphosphate kinase driven by structurally-modified ligands and active site plasticity.Nature communications · 2024Article
- Commentary on: The actin bundling activity of ITPKA mainly accounts for its migration-promoting effect in lung cancer cells.Bioscience reports · 2023Article
- The actin bundling activity of ITPKA mainly accounts for its migration-promoting effect in lung cancer cells.Bioscience reports · 2023Article
- A metabolism-related gene signature for predicting the prognosis in thyroid carcinoma.Frontiers in genetics · 2022Article
- Mechanism of BIP-4 mediated inhibition of InsP3Kinase-A.Bioscience reports · 2021Article
- Relationship of ITPKA expression with the prognosis of breast cancer.Molecular genetics & genomic medicine · 2021Article
- Inositol-triphosphate 3-kinase B confers cisplatin resistance by regulating NOX4-dependent redox balance.The Journal of clinical investigation · 2019Article
- The formin Drosophila homologue of Diaphanous2 (Diaph2) controls microtubule dynamics in colorectal cancer cells independent of its FH2-domain.Scientific reports · 2019Article
- Regulation of Hematopoietic Cell Development and Function Through Phosphoinositides.Frontiers in immunology · 2018Review
- Identification of potential therapeutic targets for gliomas by bioinformatics analysis.Oncology letters · 2017Article
- Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types.Biochemical pharmacology · 2017Review
- ITPKA expression is a novel prognostic factor in hepatocellular carcinoma.Diagnostic pathology · 2015Article
- Drosophila homologue of Diaphanous 1 (DIAPH1) controls the metastatic potential of colon cancer cells by regulating microtubule-dependent adhesion.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular migration is an essential prerequisite for metastatic dissemination of cancer cells. This study demonstrates that the neuron/testis-specific F-actin-targeted inositol 1,4,5-trisphosphate 3-kinase-A (ITPKA) is ectopically expressed in different human tumor cell lines and during tumor progression in the metastatic tumor model Balb-neuT. High expression of ITPKA increases invasive migration in vitro and metastasis in a xenograft SCID mouse model. Mechanistic studies show that ITPKA promotes migration of tumor cells by two different mechanisms as follows: growth factor independently high levels of ITPKA induce the formation of large cellular protrusions by directly modulating the actin cytoskeleton. The F-actin binding activity of ITPKA stabilizes and bundles actin filaments and thus increases the levels of cellular F-actin. In growth factor-stimulated cells, the catalytically active domain enhances basal ITPKA-induced migration by activating store-operated calcium entry through production of inositol 1,3,4,5-tetrakisphosphate and subsequent inhibition of inositol phosphate 5-phosphatase. These two functional activities of ITPKA stimulating tumor cell migration place the enzyme among the potential targets of anti-metastatic therapy.
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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.