{"id":515929,"date":"2026-03-25T17:15:00","date_gmt":"2026-03-25T09:15:00","guid":{"rendered":"https:\/\/www.um.edu.mo\/news-and-press-releases\/campus-news\/detail\/63566-2\/"},"modified":"2026-03-25T17:15:00","modified_gmt":"2026-03-25T09:15:00","slug":"63566","status":"publish","type":"post","link":"https:\/\/www.um.edu.mo\/pt-pt\/news-and-press-releases\/campus-news\/detail\/63566\/","title":{"rendered":"UM researchers reveal key to breast cancer\u2019s resistance to targeted drugs"},"content":{"rendered":"\n                        \n                        <p>A research team led by Chair Professor Chuxia Deng\nand Professor Edwin Cheung\nin the Faculty of\nHealth Sciences (FHS) at the University\nof Macau (UM) has revealed the key molecular mechanism behind resistance to the\ntargeted drug PARP inhibitors in BRCA1-deficient\nbreast cancer, providing a scientific basis for overcoming this type of drug\nresistance. The\nteam also proposed a related\ntherapeutic strategy to address this resistance. The research has been\npublished in the internationally renowned journal <i>Protein &amp; Cell<\/i>.<\/p>\n\n<p>Breast cancer is the most\ncommon malignant tumour among women worldwide, and its development is closely linked to genetic factors. About 10% of cases have a\nfamilial genetic background, most of which are caused by mutations in the BRCA1\nor BRCA2 genes. BRCA1 plays a key role in the process of DNA homologous recombination\nrepair, a repair pathway which is responsible for accurately repairing double-strand breaks and maintaining genomic\nstability. If this function is impaired, cells rely on\nother error-prone repair mechanisms, which can lead to genomic instability and cancer development. Based on this defect,\nPARP inhibitors have been developed as targeted drugs that selectively kill cancer cells with DNA repair\ndefects through a \u2018synthetic lethality\u2019 mechanism. They have now become\nan effective therapy for treating\nBRCA-mutated breast cancer. However, clinical resistance remains a major\nchallenge that limits their efficacy.<\/p>\n\n<p>To overcome drug resistance,\nthe research team has revealed a\nnew mechanism through which DNA damage\nactivates innate immune responses. DNA damage not only threatens genomic\nstability, but also generates\ncytosolic DNA fragments and abnormal double-stranded RNA (dsRNA). DNA fragments\ncan induce interferon production through the cGAS-STING pathway, thereby enhancing anti-tumour immune responses. Meanwhile, dsRNA triggers\nMAVS-mediated anti-viral mimicry\ninnate immune responses. These findings open new avenues for combination therapy involving the use of STING agonists alongside PARP inhibitors.\nAlthough the detailed mechanisms of the dsRNA-MAVS pathway are yet to be elucidated, the combination of targeted DNA repair and the activation of\nimmune responses shows promise in overcoming resistance and\nimproving breast cancer\ntreatment outcomes.<\/p>\n\n<p>Through functional proteomics, the research team\ndiscovered that PARP inhibitors can enhance the interaction between PARP1 and\nthe splicing factor SF3B1. This disrupts spliceosome\nfunction, leading to the accumulation\nof dsRNA and the activation of an anti-viral mimicry innate\nimmune response. The study also revealed a new function of BRCA1 in regulating innate immunity. BRCA1\ndeficiency leads to the\ndownregulation\nof IRF3 expression, thereby\nweakening this\nimmune response and reducing the sensitivity to PARP inhibitors, resulting in intrinsic resistance.\nNotably, the dsRNA analogue poly(I:C) can\neffectively activate this immune pathway, and combining it with PARP inhibitors significantly enhances their killing effect\non BRCA1-deficient breast cancer cells. Animal experiments confirmed that this\ncombination strategy can significantly improve the tumour suppression rate. This study elucidates a new mechanism by which BRCA1\ndeficiency leads to resistance by downregulating the IRF3-mediated\ninnate immune signalling pathway. It also puts forward the innovative approach of reversing this\nresistance by activating the pathway with poly(I:C),\nproviding a new strategy for overcoming PARP inhibitor\nresistance in BRCA1-deficient breast cancer.<\/p>\n\n<p>The corresponding authors of\nthis study are Prof\nDeng and Prof Cheung, with Zhang Cuiting, PhD candidate in UM FHS, as the first\nauthor. Other team members include Associate Professor Terence Poon Chuen Wai,\nAdjunct Associate Professor Xu Xiaoling,\nAssistant Professor Miao\nKai, and\npostdoctoral fellows Zhou Jingbo and Josh Lei Haipeng in UM FHS. The study was supported by the Natural Science\nFoundation of China (File No.: 82030094), the Science and Technology Development Fund of the Macao SAR (File Nos.:\n0009\/2022\/AKP, 0054\/2023\/RIA1, 0129\/2024\/RIA2, and 0137\/2020\/A3), and the University of Macau (File No.: MYRG-GRG2024-00073-FHS).\nThe full version of the research article is available at: <a href=\"https:\/\/academic.oup.com\/proteincell\/advance-article\/doi\/10.1093\/procel\/pwaf104\/8419885?login=false\">https:\/\/academic.oup.com\/proteincell\/advance-article\/doi\/10.1093\/procel\/pwaf104\/8419885?login=false<\/a>.<\/p>\n\n<table style=\"width: 44.7597%;height: 201px\"> <tbody> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 100.095%\" colspan=\"2\">Source: Faculty of Health Sciences<\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 56.3278%;min-width: 120px\"> <\/td> <td style=\"height: 21px;width: 43.7669%\"> <\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 100.095%\" colspan=\"2\">Media Contact Information:<\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 12px;width: 100.095%\" colspan=\"2\">Communications Office, University of Macau<\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 56.3278%;min-width: 120px\"> <\/td> <td style=\"height: 21px;width: 43.7669%\"> <\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 56.3278%;min-width: 120px\">Albee Lei<\/td> <td style=\"height: 21px;width: 43.7669%\">Tel: (853) 8822 8004<\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 56.3278%;min-width: 120px\">Bell Leong<\/td> <td style=\"height: 21px;width: 43.7669%\">Tel: (853) 8822 8009<\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 56.3278%;min-width: 120px\">Email:<\/td> <td style=\"height: 21px;width: 43.7669%\"><a href=\"mailto:prs.media@um.edu.mo\">prs.media@um.edu.mo<\/a><\/td>\n<\/tr>\n<tr style=\"height: 21px\">\n<td style=\"height: 21px;width: 56.3278%;min-width: 120px\"> <\/td> <td style=\"height: 21px;width: 43.7669%\"> <\/td> <\/tr> <tr style=\"height: 21px\"> <td style=\"height: 21px;width: 56.3278%;min-width: 120px\"><\/td><td style=\"height: 21px;width: 43.7669%\"><\/td><\/tr>\n<\/tbody>\n<\/table>\n                        \n                        ","protected":false},"excerpt":{"rendered":"<p>A research team led by Chair Professor Chuxia Deng and Professor Edwin Cheung in the Faculty of Health Sciences (FHS) at the University of Macau (UM) has revealed the key&#8230;<\/p>\n","protected":false},"author":1,"featured_media":515932,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[59],"tags":[],"class_list":["post-515929","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-campus-news"],"acf":[],"yoast_head":"<!-- This site is optimized with the 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