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MicroRNAs are short non-coding RNAs that modulate gene expression post-transcriptionally and participate in processes such as differentiation and programmed cell death. miR-32-5p is reported to exert oncogenic effects in multiple cancers, while c-MYC is a major driver of tumor growth by promoting proliferation and inhibiting apoptosis. This study evaluated how inhibiting miR-32-5p alters proliferation and apoptosis in MCF-7 breast cancer cells and assessed its relationship with c-MYC expression. Using an LNA-based inhibitor, MTT and Annexin-V/Propidium iodide analyses showed reduced viability and increased apoptosis, accompanied by significant downregulation of c-MYC mRNA, supporting a plausible regulatory pathway for therapeutic targeting.",{"@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/targeting-mir-32-5p-suppresses-c-myc-driven-proliferation-and-induces-apoptosis-in-mcf-7-breast-cancer-cells/369714/",{"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/targeting-mir-32-5p-suppresses-c-myc-driven-proliferation-and-induces-apoptosis-in-mcf-7-breast-cancer-cells/369714.png","ImageObject",300,407,{"name":92,"@type":93},"Pentious","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-27","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":52},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What was the main goal of inhibiting miR-32-5p in MCF-7 cells?","Question",{"text":112,"@type":113},"To determine how miR-32-5p inhibition affects breast tumor cell behavior, specifically apoptosis and proliferation, and to examine its relationship with c-MYC expression.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How were changes in cell viability and cell death measured?",{"text":117,"@type":113},"Cell viability was assessed using MTT assays at 24, 48, and 72 hours after transfection. Apoptotic and necrotic populations were distinguished using Annexin-V labeling with Propidium iodide.",{"name":119,"@type":110,"acceptedAnswer":120},"What effect did miR-32-5p inhibition have on c-MYC and apoptosis?",{"text":121,"@type":113},"Inhibition of miR-32-5p reduced MCF-7 viability at 48 hours and increased apoptotic cells, while also causing significant downregulation of c-MYC mRNA, indicating a plausible miR-32-5p–c-MYC regulatory relationship.","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},369714,1790766789,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":52,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},1374404730887,"https://ap-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","Medical Oncology (2025) 42:377  \n[https://doi.org/10.1007/s12032-025-02935-7](https://doi.org/10.1007/s12032-025-02935-7)  \nTargeting miR‑32‑5p suppresses c‑MYC‑driven proliferation and induces apoptosis in MCF‑7 breast cancer cells  \nAhmed I. Khoder1 · I. H. El‑Sayed2 · Yasser B. M. Ali3  \nReceived: 4 May 2025 / Accepted: 10 July 2025 / Published online: 25 July 2025 © The Author(s) 2025  \nAbstract  \nProgress in molecular medicine has resulted in novel cancer therapies, with microRNAs (miRNAs) recognized as promising instruments for cancer detection and treatment. MicroRNAs are tiny non-coding RNA sequences that manipulate gene expression at the post-transcriptional stage and are involved in cellular differentiation and death. miR-32-5p demonstratesoncogenic activity in several cancers, while c-MYC oncogene is a well-known driver of cancer, promoting tumor growth by stimulating cell proliferation, blocking apoptosis, and suppressing immune responses. This study aimed to examine how inhibiting miR-32-5p affected the behavior of breast tumor cells (MCF-7), particularly focusing on changes in cellular apoptosis and proliferation, and to investigate its relationship with c-MYC expression. A locked nucleic acid (LNA)-based inhibitor was used to knock down miR-32-5p in MCF-7 breast cancer cells. Cell viability was assessed using MTT assays at 24, 48, and 72 h post-transfection. Apoptotic and necrotic cell populations were differentiated using Annexin-V labeling with Propidium iodide. Expression levels of miR-32-5p and c-MYC were evaluated using quantitative Real-Time PCR before and after transfection with the miR-32-5p inhibitor. Inhibition of miR-32-5p significantly reduced MCF-7 cell viability at 48 h post-transfection (P \u003C 0.002) and increased apoptotic cells to approximately 17%(vs. 0.3% in controls, P\u003C 0.05), concomitant with significant downregulation of c-MYC mRNA (P \u003C 0.006). The lowest level of miR-32-5p expression was observed at 48 h following transfection, with levels gradually increasing by 72 h. This study is the first to demonstrate a plausible regulatory relationship between miR-32-5p and c-MYC in breast tumor cells. The significant reduction in cell viability and increase in apoptosis following miR-32-5p inhibition, likely mediated through c-MYC downregulation, suggests a plausible pathway that may be targeted for therapeutic intervention in breast cancer.  \n* Yasser B. M. Ali [Yasser.ali@gebri.usc.edu.eg](Yasser.ali@gebri.usc.edu.eg)  \nAhmed I. Khoder  \n[Ahmed.khodair.stu@gebri.usc.edu.eg](Ahmed.khodair.stu@gebri.usc.edu.eg);  \n[Ahmedikhoder@gmail.com](Ahmedikhoder@gmail.com)  \n[I. H. El-Sayed](I. H. El-Sayed)  \n[Ibrahimelsayed@sci.kfs.edu.eg](Ibrahimelsayed@sci.kfs.edu.eg)  \n1 Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute (GEBRI), University of Sadat City (USC), Sadat City, Egypt  \n2 Chemistry Department, Faculty of Science, Kafr ElSheikh University, Kafr El-Sheikh, Egypt  \n3 Molecular Immunology Division, Department of Molecular Biology, Genetic Engineering and Biotechnology Research Institute (GEBRI), University of Sadat City (USC), Sadat City, Egypt  \nGraphical abstract  \nKeywords Breast cancer · miR-32-5p · c-Myc · LNA · Apoptosis · Proliferation  \nAbbreviations  \nATCC American type culture collection  \nBMP5 Bone morphogenetic protein 5  \ncDNA Complementary deoxyribonucleic acid  \nc-MYC Cellular myelocytomatosis oncogene  \nΔΔCt Delta-Delta threshold cycle  \nELISA Enzyme-linked immunosorbent assay  \nFBS Fetal bovine serum  \nFITC Fluorescein isothiocyanate  \nHEPES 4-(2-Hydroxyethyl)-1-piperazineethanesul  \nfonic acid  \nHIF-1α Hypoxia-inducible factor 1-alpha  \nLNA Locked nucleic acid  \nMCF-7 Michigan cancer foundation-7 (breast can  \ncer cell line) miRNA/miR MicroRNA  \nMTT 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphe  \nnyltetrazolium bromide PBS Phosphate-buffered saline  \nPCD Programmed cell death  \nPI Propidium iodide  \nPS Phosphatidylserine  \nPTEN Phosphatase and tensin ","cbCaiiVXfKCojCW6","https://ap.wps.com/l/cbCaiiVXfKCojCW6","pdf",1722464,15,"English","# Abstract\n# Introduction\n## Rationale for miR-32-5p Investigation in Breast Cancer","[{\"question\":\"What was the main goal of inhibiting miR-32-5p in MCF-7 cells?\",\"answer\":\"To determine how miR-32-5p inhibition affects breast tumor cell behavior, specifically apoptosis and proliferation, and to examine its relationship with c-MYC expression.\"},{\"question\":\"How were changes in cell viability and cell death measured?\",\"answer\":\"Cell viability was assessed using MTT assays at 24, 48, and 72 hours after transfection. Apoptotic and necrotic populations were distinguished using Annexin-V labeling with Propidium iodide.\"},{\"question\":\"What effect did miR-32-5p inhibition have on c-MYC and apoptosis?\",\"answer\":\"Inhibition of miR-32-5p reduced MCF-7 viability at 48 hours and increased apoptotic cells, while also causing significant downregulation of c-MYC mRNA, indicating a plausible miR-32-5p–c-MYC regulatory relationship.\"}]","Targeting miR-32-5p suppresses c-MYC-driven proliferation and induces apoptosis in MCF-7 breast cancer cells | PDF",1790184188,38]