ArticleBMC cancer2016
CD44 and RHAMM are essential for rapid growth of bladder cancer driven by loss of Glycogen Debranching Enzyme (AGL).
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Intravesicular administration of sodium hyaluronate ameliorates the inflammation and cell proliferation of cystitis cystica et glandularis involving interleukin-6/JAK2/Stat3 signaling pathway.Scientific reports · 2017Trial
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- Teaching an Old Drug a New Trick: Targeting Treatment Resistance in Genitourinary Cancers.Journal of cellular signaling · 2024Article
- Frequency of pathogenic germline variants in pediatric medulloblastoma survivors.Frontiers in oncology · 2024Article
- Altered Glycosylation in Progression and Management of Bladder Cancer.Molecules (Basel, Switzerland) · 2023Review
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- Androgen Receptor Regulates CD44 Expression in Bladder Cancer.Cancer research · 2021Article
- Self-crosslinkable chitosan-hyaluronic acid dialdehyde nanoparticles for CD44-targeted siRNA delivery to treat bladder cancer.Bioactive materials · 2021Article
- Cell-specific expression of the transcriptional regulator RHAMM provides a timing mechanism that controls appropriate wound re-epithelialization.The Journal of biological chemistry · 2020Article
- The Roles of Glycans in Bladder Cancer.Frontiers in oncology · 2020Review
- Importance of PNO1 for growth and survival of urinary bladder carcinoma: Role in core-regulatory circuitry.Journal of cellular and molecular medicine · 2020Article
- Identification of Novel Glycolysis-Related Gene Signatures Associated With Prognosis of Patients With Clear Cell Renal Cell Carcinoma Based on TCGA.Frontiers in genetics · 2020Article
- Elucidating the role of Agl in bladder carcinogenesis by generation and characterization of genetically engineered mice.Carcinogenesis · 2019Article
- Glycogen debranching enzyme (AGL) is a novel regulator of non-small cell lung cancer growth.Oncotarget · 2018Article
- Expression of ganglioside GD2, reprogram the lipid metabolism and EMT phenotype in bladder cancer.Oncotarget · 2017Article
- Curcumin reversed chronic tobacco smoke exposure induced urocystic EMT and acquisition of cancer stem cells properties via Wnt/β-catenin.Cell death & disease · 2017Article
- Involvement of glycogen debranching enzyme in bladder cancer.Biomedical reports · 2017Article
- CD44: A metastasis driver and therapeutic target.Oncoscience · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundLoss of Amylo-alpha-1-6-glucosidase-4-alpha-glucanotransferase (AGL) drives rapid proliferation of bladder cancer cells by upregulating Hyaluronic acid(HA) Synthase (HAS2) mediated HA synthesis. However the role of HA receptors CD44 and Hyaluronan Mediated Motility Receptor (RHAMM) in regulating the growth of bladder cancer cells driven by loss of AGL has not been studied.
methodsWestern blot analysis and Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay was carried out to study cellular apoptosis with HAS2, CD44 and RHAMM loss in bladder cancer cells with and without AGL expression. Proliferation and softagar assays were carried out to study cellular anchorage dependent and independent growth. Clinicopathologic analysis was carried out on bladder cancer patient datasets.
resultsHigher amounts of cleaved Cas3, Cas9 and PARP was observed in AGL low bladder cancer cell with loss of HAS2, CD44 or RHAMM. TUNEL staining showed more apoptotic cells with loss of HAS2, CD44 or RHAMM in AGL low bladder cancer cells. This revealed that bladder cancer cells whose aggressive growth is mediated by loss of AGL are susceptible to apoptosis with loss of HAS2, CD44 or RHAMM. Interestingly loss of either CD44 or RHAMM induces apoptosis in different low AGL expressing bladder cancer cell lines. Growth assays showed that loss of CD44 and RHAMM predominantly inhibit anchorage dependent and independent growth of AGL low bladder cancer cells. Clinicopathologic analysis revealed that high RHAMM mRNA expression is a marker of poor patient outcome in bladder cancer and patients with high RHAMM and low AGL tumor mRNA expression have poor survival.
conclusionOur findings strongly point to the importance of the HAS2-HA-CD44/RHAMM pathway for rapid growth of bladder cancer cells with loss of AGL and provides rational for targeting this pathway at various steps for "personalized" treatment of bladder cancer patients based of their AGL expression status.
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