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AA suppresses NPC cell viability and migration, increases cleaved caspase-3, and reduces STAT3 phosphorylation while lowering claudin-1 expression. 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Knockdown of STAT3 or claudin-1 does not enhance AA’s anti-proliferative effect, but it increases AA’s anti-migratory effect.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},380115,1790367411,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,109,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":55,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":107,"slug":108},40,"healthcare",{"id":110,"doc_module":4,"doc_module_name":25,"category_name":111,"show_sort_weight":112,"slug":113},8,"Research & Report",30,"research-report",{"id":115,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},9,"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},19,"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":55,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":139,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":145},687207024478,"https://ap-avatar.wpscdn.com/davatar_a8503ba1806abce46bf441b54a3ca4cd","pharmaceuticals  \nArticle  \nAsiatic Acid Inhibits Nasopharyngeal Carcinoma Cell Viability and Migration via Suppressing STAT3 and Claudin-1  \nSupitchaya Pantia 1, Thaned Kangsamaksin 2, Tavan Janvilisri 2 and Waraporn Komyod 2, *  \nCitation: Pantia, S.; Kangsamaksin, T.; Janvilisri, T.; Komyod, W. Asiatic Acid Inhibits Nasopharyngeal Carcinoma Cell Viability and Migration via Suppressing STAT3 and Claudin-1 . Pharmaceuticals 2023, 16, 902. [https://doi.org/10.3390/](https://doi.org/10.3390/)[ ](https://doi.org/10.3390/)ph16060902  \nAcademic Editors: Paulo Santos and Lillian Barros  \nReceived: 13 May 2023  \nRevised: 5 June 2023  \nAccepted: 16 June 2023  \nPublished: 19 June 2023  \nCopyright: © 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \n1 Graduate Program in Molecular Medicine, Faculty of Science, Mahidol University, Bangkok 10400, Thailand; [supitchaya.pantia@gmail.com](supitchaya.pantia@gmail.com)  \n2 Department of Biochemistry, Faculty of Science, Mahidol University, Bangkok 10400, Thailand; [thaned.kan@mahidol.edu](thaned.kan@mahidol.edu) (T.K.); [tavan.jan@mahidol.ac.th](tavan.jan@mahidol.ac.th) (T.J.)  \n* [Correspondence: waraporn.kom@mahidol.edu](Correspondence: waraporn.kom@mahidol.edu)  \nAbstract: Nasopharyngeal carcinoma (NPC) is a prevalent cancer in Southeast Asia, but effective treatment options remain limited, and chemotherapy has a high resistance rate. Asiatic acid (AA), atriterpenoid found in Centella asiatica, has shown anticancer activity in various cancers. Therefore, this study aims to investigate the anticancer effects and mechanisms of AA in NPC cell lines. The effects of AA on NPC cytotoxicity, apoptosis, and migration were determined in TW-01 and SUNE5-8F NPC cell lines. Western blot analysis was performed to evaluate the protein expression levels affected by AA. The role of AA in proliferation and migration was investigated in STAT3 and claudin-1 knockdown cells. AA inhibited NPC cell viability and migration and induced cell death by increasing cleaved caspase-3 expression. Moreover, AA inhibited STAT3 phosphorylation and reduced claudin-1 expression in NPC cells. Although knockdown of STAT3 or claudin-1 slightly reduced cell viability, it did not enhance the anti-proliferative effect of AA. However, knockdown of STAT3 or claudin-1 increased the anti-migratory effect of AA in NPC cells. These results suggest that AA can be a promising candidate for drug development against NPC.  \nKeywords: nasopharyngeal carcinoma; asiatic acid; STAT3; claudin-1; EMT; apoptosis  \n1. Introduction  \nNasopharyngeal carcinoma (NPC) is a significant public health concern in Asia, particularly in Southeast Asia, with high incidence and mortality rates [1] . The pathogenesis of NPC is multifactorial, involving genetic, environmental, and viral factors such as Epstein–Barr virus (EBV) infection, dietary habits, and exposure to chemical agents [2] . Current treatment options for NPC are limited, with surgery being difficult due to the location of the tumor [3] . Radiotherapy is the primary treatment for NPC, with chemotherapy as a complementary option for advanced-stage cases [4] . Cisplatin-based drugs are the most effective chemotherapy for metastatic NPC; however, their use is limited due to their significant side effects, including renal, hepatic, and cardiovascular toxicity [5,6] . Therefore, the identification and development of alternative therapies with improved safety profiles are necessary to improve the management of NPC.  \nPlant-derived compounds are currently being studied for their potential use in cancer treatment. Among these natural compounds, triterpenoids have shown promising anticancer activities. Asiatic acid (AA), ","cbCaiodGchzX6OQ7","https://ap.wps.com/l/cbCaiodGchzX6OQ7","pdf",3757644,14,"English","# Introduction\n## Background and clinical challenges in NPC\n## Rationale for plant-derived triterpenoids and AA\n## JAK/STAT3 signaling and metastasis relevance in NPC","[{\"question\":\"What is the main purpose of this study on asiatic acid (AA) in NPC?\",\"answer\":\"To investigate AA’s anticancer effects and mechanisms in NPC cell lines, focusing on cytotoxicity, apoptosis, and migration pathways.\"},{\"question\":\"How does AA affect NPC cell viability, apoptosis, and migration?\",\"answer\":\"AA inhibits NPC cell viability and migration and induces cell death by increasing cleaved caspase-3 expression.\"},{\"question\":\"What roles do STAT3 and claudin-1 play in AA’s anti-NPC actions?\",\"answer\":\"AA reduces STAT3 phosphorylation and lowers claudin-1 expression. Knockdown of STAT3 or claudin-1 does not enhance AA’s anti-proliferative effect, but it increases AA’s anti-migratory effect.\"}]","Asiatic Acid Inhibits Nasopharyngeal Carcinoma Cell Viability and Migration via Suppressing STAT3 and Claudin-1 | PDF",1790238795,35]