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DNMT1-driven epigenetic silencing is intensified by competing interactions with long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), forming regulatory networks. Functionally, miR-152 suppresses tumors via pathways including PI3K/AKT/mTOR, EMT, and chemoresistance, though effects can be context-dependent, showing dual roles in prostate cancer and some leukemias. Therapeutic restoration using mimics, demethylating agents, or nanocarrier delivery is promising in preclinical studies, motivating clinical exploration.",{"@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":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/regulation-and-function-of-microrna-152-in-various-types-of-cancers-its-upstream-regulators-and-downstream-targets/366170/",{"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/regulation-and-function-of-microrna-152-in-various-types-of-cancers-its-upstream-regulators-and-downstream-targets/366170.png","ImageObject",300,407,{"name":92,"@type":93},"Nguyễn Văn Học","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":39},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"How does miR-152 regulate gene expression in cancer?","Question",{"text":112,"@type":113},"miR-152 binds the 3′-UTR of target mRNAs, modulating protein expression and influencing cancer progression. Its activity is shaped by epigenetic and RNA-network mechanisms.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What leads to miR-152 downregulation in many cancers?",{"text":117,"@type":113},"Promoter hypermethylation is highlighted as a primary mechanism, mediated by DNMT1. This epigenetic silencing is further reinforced by lncRNA and circRNA competitive sponging.",{"name":119,"@type":110,"acceptedAnswer":120},"What therapeutic strategies target miR-152 for cancer treatment?",{"text":121,"@type":113},"The review describes restoring miR-152 expression using miRNA mimics, demethylating agents, and nanocarrier-based delivery systems. 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Among these, microRNA-152 (miR-152) is frequently downregulated in diverse malignancies—including breast, endometrial, gastrointestinal, and hematologic cancers—primarily due to promoter hypermethylation. This epigenetic silencing, mediated by DNMT1, is compounded by competitive sponging from long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), forming intricate regulatory networks. Functionally, miR-152 acts as a tumor suppressor by targeting oncogenic pathways such as PI3K/AKT/mTOR, EMT drivers, and chemoresistance mediators. However, its role is context-dependent, exhibiting dual oncogenic and suppressive effects in prostate cancer and certain leukemias. Therapeutically, restoring miR-152 expression via mimics, demethylating agents, or nanocarrier-based delivery systems shows promise in preclinical studies for reversing chemoresistance and inhibiting metastasis. This review synthesizes miR-152’s upstream regulators, downstream targets, and clinical potential, offering aroadmap for its exploitation in precision oncology.  \nKeywords Noncoding RNAs · MicroRNA-152 · MiR-152 · Cancers  \n* Abdollah Jafarzadeh [Jafarzadeh14@yahoo.com](Jafarzadeh14@yahoo.com)  \n* Fatemeh Divani [fatemehdivani@gmail.com](fatemehdivani@gmail.com)  \n* Hamed Mirzaei  \n[mirzaei-h@kaums.ac.ir](mirzaei-h@kaums.ac.ir); [h.mirzaei2002@gmail.com](h.mirzaei2002@gmail.com)  \n1 Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran  \n2 Applied Cellular and Molecular Research Center, Kerman University of Medical Sciences, Kerman, Iran  \n3 Department of Immunology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran  \n4 Department of Hematology and Laboratory Sciences, School of Para-Medicine, Kerman University of Medical Sciences, Kerman, Iran  \n5 Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran  \n6 Chronic Respiratory Diseases Research Center (CRDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran  \n7 Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran 14778-93855, Iran  \n8 Department of Rheumatology, School of Medicine, Imam Khomeini Hospital, Tehran University of Medical Sciences, Tehran, Iran  \n9 Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran  \n10 Student Research Committee, Kashan University of Medical Sciences, Kashan, Iran  \nIntroduction  \nAmong noncoding RNAs (ncRNAs)ncRNAs—microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs)—miRNAs (~ 22 nt) are the most extensively characterized. MiRNAs canonically target the 3 ′-untranslated region (3 ′-UTR) of mRNAs, thereby inhibiting the expression of their target proteins [1] . However, miRNAs can also interact with other genetic elements, such as gene promoters, coding sequences, and 5 ′-UTRs [1]. lncRNAs, which contain >200 nt, regulate miRNAs by acting as competing endogenous RNAs (ceRNAs) that inhibit miRNA binding to their targets [2] . Similarly, circular RNAs function as miRNA sponges, pre","cbCaiv4VeD17YHry","https://ap.wps.com/l/cbCaiv4VeD17YHry","pdf",2112962,"English","# Abstract\n# Introduction\n# Role of miR‑152 in specific cancer types\n## Breast cancer","[{\"question\":\"How does miR-152 regulate gene expression in cancer?\",\"answer\":\"miR-152 binds the 3′-UTR of target mRNAs, modulating protein expression and influencing cancer progression. Its activity is shaped by epigenetic and RNA-network mechanisms.\"},{\"question\":\"What leads to miR-152 downregulation in many cancers?\",\"answer\":\"Promoter hypermethylation is highlighted as a primary mechanism, mediated by DNMT1. This epigenetic silencing is further reinforced by lncRNA and circRNA competitive sponging.\"},{\"question\":\"What therapeutic strategies target miR-152 for cancer treatment?\",\"answer\":\"The review describes restoring miR-152 expression using miRNA mimics, demethylating agents, and nanocarrier-based delivery systems. These approaches are reported to show preclinical potential for reversing chemoresistance and limiting metastasis.\"}]","Regulation and function of microRNA-152 in various types of cancers - its upstream regulators and downstream targets | PDF",1790164044]