ArticleMolecular biology of the cell2001
Hyaluronan activates cell motility of v-Src-transformed cells via Ras-mitogen-activated protein kinase and phosphoinositide 3-kinase-Akt in a tumor-specific manner.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 97 citations in OpenAlex.
- The protective role of CD44 and microRNA-146a in tendinopathy.Bone & joint research · 2026Article
- Expression and molecular characterization of an intriguing hyaluronan synthase (HAS) from the symbiont "PeerJ · 2025Article
- Hyaluronic acid: Function and location in the urothelial barrier for bladder pain syndrome/interstitial cystitis, an in vitro study.PloS one · 2025Article
- Article
- Redox and Inflammatory Signaling, the Unfolded Protein Response, and the Pathogenesis of Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Article
- Activity of two hyaluronan preparations on primary human oral fibroblasts.Journal of periodontal research · 2019Article
- Novel agents for pancreatic ductal adenocarcinoma: emerging therapeutics and future directions.Journal of hematology & oncology · 2018Review
- Complex roles of the stroma in the intrinsic resistance to gemcitabine in pancreatic cancer: where we are and where we are going.Experimental & molecular medicine · 2017Review
- Soft Substrates Containing Hyaluronan Mimic the Effects of Increased Stiffness on Morphology, Motility, and Proliferation of Glioma Cells.Biomacromolecules · 2017Article
- Role of hyaluronan in pancreatic cancer biology and therapy: Once again in the spotlight.Cancer science · 2016Review
- Targeting hyaluronan for the treatment of pancreatic ductal adenocarcinoma.Acta pharmaceutica Sinica. B · 2016Review
- Interactions between Hyaluronan and Its Receptors (CD44, RHAMM) Regulate the Activities of Inflammation and Cancer.Frontiers in immunology · 2015Review
- 4-Methylumbelliferone inhibits ovarian cancer growth by suppressing thymidine phosphorylase expression.Journal of ovarian research · 2014Article
- CD44 and hyaluronan promote the bone morphogenetic protein 7 signaling response in murine chondrocytes.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Intracellular domain fragment of CD44 alters CD44 function in chondrocytes.The Journal of biological chemistry · 2013Article
- Effects of hyaluronic acid and CD44 interaction on the proliferation and invasiveness of malignant pleural mesothelioma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- The role of a new CD44st in increasing the invasion capability of the human breast cancer cell line MCF-7.BMC cancer · 2011Article
- Hyaluronan stabilizes focal adhesions, filopodia, and the proliferative phenotype in esophageal squamous carcinoma cells.The Journal of biological chemistry · 2010Article
- Cellular processes of v-Src transformation revealed by gene profiling of primary cells--implications for human cancer.BMC cancer · 2010Article
- Tumor necrosis factor-alpha regulates transforming growth factor-beta-dependent epithelial-mesenchymal transition by promoting hyaluronan-CD44-moesin interaction.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the production of hyaluronan (HA) and its effect on cell motility in cells expressing the v-src mutants. Transformation of 3Y1 by v-src virtually activated HA secretion, whereas G2A v-src, a nonmyristoylated form of v-src defective in cell transformation, had no effect. In cells expressing the temperature-sensitive mutant of v-Src, HA secretion was temperature dependent. In addition, HA as small as 1 nM, on the other side, activated cell motility in a tumor-specific manner. HA treatment strongly activated the motility of v-Src-transformed 3Y1, whereas it showed no effect on 3Y1- and 3Y1-expressing G2A v-src. HA-dependent cell locomotion was strongly blocked by either expression of dominant-negative Ras or treatment with a Ras farnesyltransferase inhibitor. Similarly, both the MEK1 inhibitor and the kinase inhibitor clearly inhibited HA-dependent cell locomotion. In contrast, cells transformed with an active MEK1 did not respond to the HA. Finally, an anti-CD44-neutralizing antibody could block the activation of cell motility by HA as well as the HA-dependent phosphorylation of mitogen-activated protein kinase and Akt. Taken together, these results suggest that simultaneous activation of the Ras-mitogen-activated protein kinase pathway and the phosphoinositide 3-kinase pathway by the HA-CD44 interaction is required for the activation of HA-dependent cell locomotion in v-Src-transformed cells.
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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 Socratic graph.