{"id":4493,"date":"2021-12-13T17:22:38","date_gmt":"2021-12-14T01:22:38","guid":{"rendered":"https:\/\/keck.usc.edu\/news\/a-new-function-of-cardiac-glycosides\/"},"modified":"2025-02-28T14:05:40","modified_gmt":"2025-02-28T22:05:40","slug":"a-new-function-of-cardiac-glycosides","status":"publish","type":"post","link":"https:\/\/keck.usc.edu\/news\/a-new-function-of-cardiac-glycosides\/","title":{"rendered":"A new function of cardiac glycosides"},"content":{"rendered":"\n \n \n\n\n\n\n\n\n\n
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\n\n \n Press Release<\/span>\n\n\n\n<\/div>\n \n \n
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A new function of cardiac glycosides<\/h1>\n\n\n<\/div>\n \n \n
\n \n December 13, 2021<\/span>\n <\/div>\n \n \n
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Published in the journal Neoplasia, USC Norris member Dr. Amy Lee and her colleagues revealed (CGs), medications used to treat the heart and related conditions, as an inhibitor of stress induction of GRP78, a glucose-regulated protein. These findings support further investigation into CGs as a potential new treatment option for pancreatic and other cancers that depend on GRP78 for growth and survival. Read the full publication here: https:\/\/pubmed.ncbi.nlm.nih.gov\/34768108\/<\/a>.<\/p>\n\n\n\n<\/div>\n <\/div>\n\n\n <\/div><\/div>\n","protected":false},"excerpt":{"rendered":"","protected":false},"author":168,"featured_media":4494,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"advgb_blocks_editor_width":"","advgb_blocks_columns_visual_guide":"","footnotes":"","_links_to":"","_links_to_target":""},"categories":[6],"tags":[532],"class_list":["post-4493","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-press-release","tag-department-of-cancer-biology"],"acf":[],"yoast_head":"\nA new function of cardiac glycosides<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/keck.usc.edu\/news\/a-new-function-of-cardiac-glycosides\/\" \/>\n<meta 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