Paraskevi Heldin research group
We aim to investigate the molecular mechanisms that lead to excessive hyaluronan accumulation in certain tumors and infections, resulting in the over-activity of CD44 signaling. Such knowledge is crucial for better management of metastasis and infections.
Targeting hyaluronan-CD44 signaling in cancer and infection
During tumor progression, cell surface molecules such as CD44 function as microenvironmental sensors functioning as metastasis suppressors or promoters in a cellular context. Our research focus on the growth factor-mediated induced hyaluronan-CD44 signaling during inflammation, cancer and infection. We found that increased hyaluronan synthase 2 (HAS2)-synthesized hyaluronan activated CD44 signaling during Dengue virus infection-induced inflammation, disrupting endothelial integrity. Increased serum hyaluronan levels are an early predictor of warning signs for severe dengue virus infection. In certain tumors, such as gliomas, a CD44/hyaluronan feedback circuit drives tumor progression, and is related to the expression of PDGF and PDGF receptor family members.
Group members
Publications
A biological guide to glycosaminoglycans: current perspectives and pending questions
Part of The FEBS Journal, p. 3331-3366, 2024
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Hyaluronan-Induced CD44-iASPP Interaction Affects Fibroblast Migration and Survival
Part of Cancers, 2023
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CD44 Depletion in Glioblastoma Cells Suppresses Growth and Stemness and Induces Senescence
Part of Cancers, 2022
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Part of Scientific Reports, 2022
- DOI for Hyaluronan nanoscale clustering and Hyaluronan synthase 2 expression are linked to the invasion of child fibroblasts and infantile fibrosarcoma in vitro and in vivo
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Part of Cancers, 2022
- DOI for Identification of a Small Molecule Inhibitor of Hyaluronan Synthesis, DDIT, Targeting Breast Cancer Cells
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