{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["Perconti G"],"pubmed_abstract":["Cell surface expression of alpha-enolase, a glycolytic enzyme displaying moonlighting activities, has been shown to contribute to the motility and invasiveness of cancer cells through the protein non-enzymatic function of binding plasminogen and enhancing plasmin formation. Although a few recent records indicate the involvement of protein partners in the localization of alpha-enolase to the plasma membrane, the cellular mechanisms underlying surface exposure remain largely elusive. Searching for novel interactors and signalling pathways, we used low-metastatic breast cancer cells, a doxorubicin-resistant counterpart and a non-tumourigenic mammary epithelial cell line. Here, we demonstrate by a combination of experimental approaches that epidermal growth factor (EGF) exposure, like lipopoly"],"journal":["Scientific reports"],"pagination":["3841"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5476664"],"repository":["biostudies-literature"],"pubmed_title":["Pro-invasive stimuli and the interacting protein Hsp70 favour the route of alpha-enolase to the cell surface."],"pmcid":["PMC5476664"],"pubmed_authors":["Perconti G","Maranto C","Romancino DP","Rubino P","Giallongo A","Bongiovanni A","Feo S"],"additional_accession":[]},"is_claimable":false,"name":"Pro-invasive stimuli and the interacting protein Hsp70 favour the route of alpha-enolase to the cell surface.","description":"Cell surface expression of alpha-enolase, a glycolytic enzyme displaying moonlighting activities, has been shown to contribute to the motility and invasiveness of cancer cells through the protein non-enzymatic function of binding plasminogen and enhancing plasmin formation. Although a few recent records indicate the involvement of protein partners in the localization of alpha-enolase to the plasma membrane, the cellular mechanisms underlying surface exposure remain largely elusive. Searching for novel interactors and signalling pathways, we used low-metastatic breast cancer cells, a doxorubicin-resistant counterpart and a non-tumourigenic mammary epithelial cell line. Here, we demonstrate by a combination of experimental approaches that epidermal growth factor (EGF) exposure, like lipopoly","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jun","modification":"2025-04-25T19:22:16.1Z","creation":"2019-03-27T02:47:58Z"},"accession":"S-EPMC5476664","cross_references":{"pubmed":["28630480"],"doi":["10.1038/s41598-017-04185-8"]}}