[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-332714-105":59,"doc-detail-332714-en":130},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":123,"head_meta":125,"extra_data":127,"updated_unix":129},105,"en","protein-rna-interaction-dynamics-reveal-key-regulators-of-oncogenic-kras-driven-cancers","Protein-RNA interaction dynamics reveal key regulators of oncogenic KRAS-driven cancers","","Oncogenic KRAS mutations rewire cellular signaling and contribute to cancer development, yet how they reshape post-transcriptional regulatory networks governed by RNA-binding proteins (RBPs) remains unclear. This study systematically dissects KRAS-driven changes in RNA–RBP interactions using the mRNA interactome capture approach in lung isogenic cell lines. It identifies 35 cancer-associated RBPs with increased or decreased RNA binding upon KRAS activation, including PDCD11 and ELAVL2, linking RNA-binding dynamics to survival and migration in KRAS mutant tumors. The results provide a resource for mapping RBP regulatory networks and informing therapeutic strategies targeting KRAS-driven malignancies.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/protein-rna-interaction-dynamics-reveal-key-regulators-of-oncogenic-kras-driven-cancers/332714/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/protein-rna-interaction-dynamics-reveal-key-regulators-of-oncogenic-kras-driven-cancers/332714.png","ImageObject",300,407,{"name":92,"@type":93},"Skyler","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-23","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":29},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What question does the study address about oncogenic KRAS mutations?","Question",{"text":112,"@type":113},"It investigates how oncogenic KRAS reshapes post-transcriptional regulatory networks mediated by RNA-binding proteins (RBPs).","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What method is used to measure RNA-bound RBPs in KRAS-mutant lung models?",{"text":117,"@type":113},"The study uses the mRNA interactome capture (RIC) approach, implemented via formaldehyde crosslinking combined with RNA interactome capture (FAX-RIC).",{"name":119,"@type":110,"acceptedAnswer":120},"How many cancer-associated RBPs are identified, and what do the findings represent?",{"text":121,"@type":113},"The study identifies 35 cancer-associated RBPs showing significantly altered RNA binding upon oncogenic KRAS activation, with examples including PDCD11 and ELAVL2.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},332714,1790193034,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":29,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":52,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":144,"preview_page_count":4},2336464648746,"https://ap-avatar.wpscdn.com/davatar_276721f389ce27ea32af1340a28f341c","[www. nature.com/scientificreports](www. nature.com/scientificreports)  \nOPEN  \nProtein-RNA interaction dynamics reveal key regulators of oncogenic KRAS-driven cancers  \nKa-Yun Ban1, Yong-woo Na3, Juhan Song1, Jong-Seo Kim3 & Jimi Kim1,2􀀍  \nKRAS is one of the most frequently mutated oncogenes across various cancers. Oncogenic KRAS mutations rewire cellular signaling, leading to significant alterations in gene expression. RNA-binding proteins (RBPs) play a pivotal role in gene expression regulation by post-transcriptionally controlling various aspects of RNA metabolism. It has become clear that interactions between RBPs and RNA are frequently dysregulated in numerous cancers. However, how oncogenic KRAS mutations reshape the post-transcriptional regulatory network mediated by RBPs remains poorly understood. In this study, we systematically dissected oncogenic KRAS-driven alterations of RNA-RBP networks. We identified 35 cancer-associated RBPs with either increased or decreased RNA binding upon oncogenic KRAS activation, including PDCD11, which is essential for the viability of KRAS mutant cancers, and ELAVL2, which regulates cell migration in KRAS mutant lung cancers. Our study serves as a crucial resource for elucidating RBP regulatory networks in KRAS mutant cancers and may provide new avenues for therapeutic strategies targeting KRAS mutant malignancies.  \nPost-transcriptional regulation, encompassing mRNA processing, mRNA transport, mRNA stability, and translational regulation, plays a pivotal role in gene expression1. RNA-binding proteins (RBPs) are key posttranscriptional regulators, dictating the function and fate of mRNAs at every stage of post-transcriptional regulation2,3. An accumulating body of evidence suggests that RBPs are dysregulated in cancers, playing critical roles in various aspects of cancer biology including cancer development, invasion, metastasis, and resistance to cancer therapy4–7. The identification of cancer-associated RBPs has primarily relied on gene expression profiling, leveraging transcriptome data to discern RBPs that are upregulated or downregulated in cancers compared to normal tissues. However, transcript levels do not always correlate with protein abundance, and the total abundance of RBPs does not reflect RNA-bound RBPs (active RBPs) . Thus, variations at the transcript level may not accurately represent alterations in the RNA-bound RBPs8–10. Therefore, studies on dynamic RNA interactions with RBPs are crucial to fully understand the impact of RBP-mediated post-transcriptional regulation on cancer development.  \nKRAS is one of the most frequently mutated oncogenes in various human cancers. In particular, its mutation occurs in 20–40% of non-small cell lung cancer (NSCLC), with TP53 mutation often identified as a co-mutation11–13. KRAS mutation leads to constitutive activation of several downstream signaling pathways, including RAF/MAPK and PI3K/AKT, which are involved in cell growth, differentiation, and survival14. This in turn results in significant gene expression changes, promoting malignant transformation15. Furthermore, the gene expression changes in cancer can also result from aberrant post-transcriptional regulation16, 17. However, the mechanisms through which oncogenic KRAS mutations reshape the post-transcriptional regulatory network, particularly those involving RBPs, are not fully understood. A recent study has demonstrated that oncogenic KRAS dynamically modulates a network of RBPs including nucleolin to induce cell proliferation and tumorigenesis18. This modulation was observed in the context of whole transcriptome interactions governed by ERK signaling, downstream ofKRAS, in pancreatic cancers. Nevertheless, our understanding of the changes in the mRNA interactome in response to oncogenic KRAS, particularly in lung cancer and other cancer types, is still limited.  \nIn this study, we systematically examined RNA-bound RBPs in lung isogenic cell lines with KRAS mutation using ","cbCair7o3fdJg0bD","https://ap.wps.com/l/cbCair7o3fdJg0bD","pdf",5325203,"English","# Results\n## RNA binding landscape changes during oncogenic KRAS-driven tumorigenesis","[{\"question\":\"What question does the study address about oncogenic KRAS mutations?\",\"answer\":\"It investigates how oncogenic KRAS reshapes post-transcriptional regulatory networks mediated by RNA-binding proteins (RBPs).\"},{\"question\":\"What method is used to measure RNA-bound RBPs in KRAS-mutant lung models?\",\"answer\":\"The study uses the mRNA interactome capture (RIC) approach, implemented via formaldehyde crosslinking combined with RNA interactome capture (FAX-RIC).\"},{\"question\":\"How many cancer-associated RBPs are identified, and what do the findings represent?\",\"answer\":\"The study identifies 35 cancer-associated RBPs showing significantly altered RNA binding upon oncogenic KRAS activation, with examples including PDCD11 and ELAVL2.\"}]","Protein-RNA interaction dynamics reveal key regulators of oncogenic KRAS-driven cancers | PDF",1789999182,25]