ArticleJournal of oncology2012
HAX1 Augments Cell Proliferation, Migration, Adhesion, and Invasion Induced by Urokinase-Type Plasminogen Activator Receptor.
Article in Journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- HAX1 impact on collective cell migration, cell adhesion, and cell shape is linked to the regulation of actomyosin contractility.Molecular biology of the cell · 2019Article
- Prognostic value of urokinase plasminogen activator system in non-small cell lung cancer: A systematic review and meta-analysis.Molecular and clinical oncology · 2018Article
- β-Catenin Knockdown Affects Mitochondrial Biogenesis and Lipid Metabolism in Breast Cancer Cells.Frontiers in physiology · 2017Article
- Expression of HAX1 and Ki-67 in breast cancer and its correlations with patient's clinicopathological characteristics and prognosis.International journal of clinical and experimental medicine · 2015Article
- Prognostic role of urokinase plasminogen activator receptor in gastric and colorectal cancer: A systematic review and meta-analysis.OncoTargets and therapy · 2015Review
- Human Sprouty1 suppresses growth, migration, and invasion in human breast cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Hax-1 is required for Rac1-Cortactin interaction and ovarian carcinoma cell migration.Genes & cancer · 2014Article
- SPRY1 promotes the degradation of uPAR and inhibits uPAR-mediated cell adhesion and proliferation.American journal of cancer research · 2014Article
- Human sprouty1 suppresses urokinase receptor-stimulated cell migration and invasion.ISRN biochemistry · 2013Article
- The critical role of dysregulated FOXM1-PLAUR signaling in human colon cancer progression and metastasis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Comment on "HAX1 Augments Cell Proliferation, Migration, Adhesion, and Invasion Induced by Urokinase-Type Plasminogen Activator Receptor".Journal of oncology · 2013Article
- Differential roles of uPAR in peritoneal ovarian carcinomatosis.Neoplasia (New York, N.Y.) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The urokinase-type plasminogen activator receptor (uPAR) is a cell surface receptor which has a multifunctional task in the process of tumorigenesis including cell proliferation, adhesion, migration, and invasion. Many of the biological functions of uPAR necessitate interactions with other proteins. We have shown previously that uPAR interacts with HAX1 protein (HS-1-associated protein X-1). In the current study, to gain insight into the possible role of HAX1 overexpression in regulation of uPAR signal transduction pathway, several function assays were used. We found that, upon stimulation of uPAR, HAX1 colocalizes with uPAR suggesting a physiological role for HAX1 in the regulation of uPAR signal transduction. HAX1 overexpression augments cell proliferation and migration in uPAR-stimulated cells. Moreover, HAX1 over-expression augmented uPAR-induced cell adhesion to vitronectin as well as cellular invasion. Our results suggest that HAX1 over-expression may underlay a novel mechanism to regulate uPAR-induced functions in cancer cells.
Identifiers
What OpenQuestion holds
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.