{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dai L"],"funding":["Ladies Leukemia League","Department of Defense Career Development Award","NCRR NIH HHS","National Natural Science Foundation of China","NCI NIH HHS","National Institutes of Health"],"pagination":["158-66"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4410079"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["362(2)"],"pubmed_abstract":["Kaposi sarcoma-associated herpesvirus (KSHV) is the etiologic agent for Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL), malignancies arising primarily in immunocompromised patients particularly AIDS-patients, which still lack effective therapy. Hyaluronan (HA) is a large glucuronic acid and has been found closely related to multiple functions in cancer cells, although its role in viral oncogenesis remains largely unknown. Here we provide first evidence that KSHV de novo infection induces HA production from primary endothelial cells through upregulation of HA synthase gene 1 (Has1) and a multifunctional glycoprotein, CD147. Further data demonstrate that KSHV-induced HA production requires viral latent protein, LANA (in particular functional domain A) and MAPK/ERK signaling activities. In functions, HA production is necessary for KSHV/LANA-induced primary endothelial cell invasion, a hallmark feature for KS development. For clinical relevance, our data indicate that the KSHV+ group has higher levels of HA and Has1 activities in its plasma than the KSHV- group of cohort HIV-infected patients. Together, our findings provide innovative insights into the mechanisms of oncogenic virus activation of HA production and its role in virus-associated malignancy pathogenesis, which may help to develop novel therapeutic strategies by targeting HA and related signaling."],"journal":["Cancer letters"],"pubmed_title":["Induction of hyaluronan production by oncogenic KSHV and the contribution to viral pathogenesis in AIDS patients."],"pmcid":["PMC4410079"],"funding_grant_id":["R01 CA082867","81221001","P20-RR021970-06","R01-CA142362","81472547","R01-CA082867","R01 CA142362","P20 RR021970","81272191","81101791","2014-2015","CA140437","81400164"],"pubmed_authors":["Dai L","Qin Z","Bonstaff K","Chen Y","Toole B","Parsons C","Doyle L"],"additional_accession":[]},"is_claimable":false,"name":"Induction of hyaluronan production by oncogenic KSHV and the contribution to viral pathogenesis in AIDS patients.","description":"Kaposi sarcoma-associated herpesvirus (KSHV) is the etiologic agent for Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL), malignancies arising primarily in immunocompromised patients particularly AIDS-patients, which still lack effective therapy. Hyaluronan (HA) is a large glucuronic acid and has been found closely related to multiple functions in cancer cells, although its role in viral oncogenesis remains largely unknown. Here we provide first evidence that KSHV de novo infection induces HA production from primary endothelial cells through upregulation of HA synthase gene 1 (Has1) and a multifunctional glycoprotein, CD147. Further data demonstrate that KSHV-induced HA production requires viral latent protein, LANA (in particular functional domain A) and MAPK/ERK signaling activities. In functions, HA production is necessary for KSHV/LANA-induced primary endothelial cell invasion, a hallmark feature for KS development. For clinical relevance, our data indicate that the KSHV+ group has higher levels of HA and Has1 activities in its plasma than the KSHV- group of cohort HIV-infected patients. Together, our findings provide innovative insights into the mechanisms of oncogenic virus activation of HA production and its role in virus-associated malignancy pathogenesis, which may help to develop novel therapeutic strategies by targeting HA and related signaling.","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Jul","modification":"2025-05-29T19:38:38.195Z","creation":"2019-03-27T01:50:32Z"},"accession":"S-EPMC4410079","cross_references":{"pubmed":["25837851"],"doi":["10.1016/j.canlet.2015.03.034"]}}