[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-332136-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-332136-en":131},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","pdl1-targeting-by-mir-138-5p-amplifies-anti-tumor-immunity-and-jurkat-cells-survival-in-non-small-cell-lung-cancer","PDL1 targeting by miR-138-5p amplifies anti-tumor immunity and Jurkat cells survival in non-small cell lung cancer","","Non-small cell lung cancer (NSCLC) accounts for most lung cancer cases and remains associated with poor prognosis despite limited efficacy of standard therapies. The study investigates how miR-138-5p modulates the PD-1/PD-L1 immune checkpoint axis by impairing PD-L1 expression in adenocarcinoma cell lines. Bioinformatics identified dysregulated miRNAs linked to hsa-miR-138 and CD274 mRNA. Functional experiments show miR-138-5p alters PD-L1-related regulation, cell proliferation, and survival, including Jurkat cell exhaustion dynamics under cytokine-stimulated conditions.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & Report",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/pdl1-targeting-by-mir-138-5p-amplifies-anti-tumor-immunity-and-jurkat-cells-survival-in-non-small-cell-lung-cancer/332136/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/pdl1-targeting-by-mir-138-5p-amplifies-anti-tumor-immunity-and-jurkat-cells-survival-in-non-small-cell-lung-cancer/332136.png","ImageObject",300,407,{"name":42,"@type":43},"Hazel","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-26","2026-09-21",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",12,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"Why is the PD-1/PD-L1 pathway important in NSCLC immune evasion?","Question",{"text":63,"@type":64},"PD-1 and PD-L1 act as co-inhibitory checkpoint molecules that tumors use to escape CD8+ T-cell killing. Their interaction promotes T-cell dysfunction, exhaustion, apoptosis, and reduced anti-tumor activity.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What role does miR-138-5p play in regulating PD-L1?",{"text":68,"@type":64},"The study evaluates miR-138-5p as a regulator that targets the CD274 (PD-L1) axis. By impairing PD-L1 expression, miR-138-5p is examined for effects on immune escape and downstream cellular responses.",{"name":70,"@type":61,"acceptedAnswer":71},"How were Jurkat cells used to assess anti-tumor immunity effects?",{"text":72,"@type":64},"Jurkat cells and NSCLC cell lines were cultured under cytokine stimulation to model cancer environmental conditions. The experiments assess how miR-138-5p preserves Jurkat cell survival by modulating the PD-L1/PD-1 pathway and related exhaustion effects.","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},332136,1790169145,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,111,115,120,123,127],{"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":107,"doc_module":4,"doc_module_name":25,"category_name":108,"show_sort_weight":109,"slug":110},7,"Healthcare",40,"healthcare",{"id":112,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":113,"slug":114},8,30,"research-report",{"id":116,"doc_module":4,"doc_module_name":25,"category_name":117,"show_sort_weight":118,"slug":119},9,"Religion & Spirituality",20,"religion-spirituality",{"id":118,"doc_module":4,"doc_module_name":25,"category_name":121,"show_sort_weight":118,"slug":122},"World Cup","world-cup",{"id":124,"doc_module":4,"doc_module_name":25,"category_name":125,"show_sort_weight":124,"slug":126},10,"Lifestyle","lifestyle",{"id":128,"doc_module":4,"doc_module_name":25,"category_name":129,"show_sort_weight":97,"slug":130},19,"General","general",{"code":4,"msg":82,"data":132},{"doc_id":79,"user_id":133,"nickname":42,"user_avatar":134,"doc_module":4,"category_id":112,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":140,"language":141,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":12,"update_tm":145,"read_time":146,"preview_page_count":4},137441390410,"https://ap-avatar.wpscdn.com/avatar/2000252f4ab5702993?_k=1776741390130283984","[www. nature.com/scientificreports](www. nature.com/scientificreports)  \nOPEN  \nPDL1 targeting by miR‑138‑5p amplifies anti‑tumor immunity and Jurkat cells survival in non‑small cell lung cancer  \nFatemeh Rostami1, ZahraTavakol Hamedani2, Azadeh Sadoughi3, Marzieh Mehrabadi1 & Fatemeh kouhkan1*  \nNon‑small cell lung cancer (NSCLC) has constituted over 80% of the lung cancer population with a poor prognosis. Over the past decade, immunotherapy has been constructed in the enlargement of immune checkpoint inhibitors as a promising approach for NSCLC treatment. Evading the immune system using the PD‑1/PD‑L1 axis is an intelligent way for cancers, and T cells cannot respond fully and confront cancer. Recently, the miR‑138 was reported as a PD‑L1 regulator in NSCLC. However, its inhibitory impact onT‑cell exhaustion has not been characterized. The present study aims to impair PD‑L1 (B7‑H1) expression inAdenocarcinoma cell lines using miR‑138‑5p and determines how it prevents Jurak cell exhaustion. To gain the purpose, first, 18 highly significant dysregulated miRNAs containing hsa‑miR‑138 and CD274‑mRNA network were detected in NSCLC based on bioinformatics analysis. Moreover, our study revealed a high level of miR‑138‑5p could make significant changes like PDL1 downregulation, proliferation, and mortality rate inA549/Calu6 cells. We also simulate cancer environmental conditions by culturing Jurak cells and NSCLC cell lines under the influence of stimulator cytokines to show how miR‑138‑5p survives Jurak cells by targeting PD‑L1/PD‑1pathway.  \nKeywords NSCLC, miR-138-5p, PD-L1/PD-1, Jurak, A549, Calu6, Cytokine  \nLung cancer containing Non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma (SCLC) subtypes is one of the leading causes of cancer-related deaths worldwide1. NSCLC, which has nearly 85% of the lung cancer population, has a poor prognosis, disappointing standard therapies, and a low survival rate2. Thus, improving understanding of the complexity and mechanism involved in anti-tumor immunity in parallel with molecular changes could be useful in the evolution of cancer biology and tumor immunotherapy. In normal circumstances, the series of co-inhibitory and co-stimulatory receptors are involved in protecting the host against autoimmune and infectious diseases with engagement with their ligand3,4. Moreover, collecting proof illustrated that tumors have used these pathways as an intelligent and crucial mechanism to escape from the anti-tumor immune system and subsequently progress and metastasis5,6. Among those co-inhibitory pathways (receptor and ligand), programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PDL1) play a vital role as an instrument in immune escaping that is used by cancer cells6. Interestingly, in recent decades researchers developed some drugs such as Nivolumab7 and pembrolizumab8,9 as immune checkpoint inhibitors that have blocked the PD1-PDL1 pathway. PD1(also known as CD279) is a transmembrane receptor and apoptosis-associated molecule10 that was known as a negative regulator of immune response by studying Nishimura and colleagues on PD1-defective mice11 and expressed in T cells in peripheral tissues. PD-L1 (also known as B7-H1 or CD274) is a member of the B7-H1 transmembrane receptor family encoded by the CD274 gene located on chromosome 9 in the human genome12, and it is generally expressed on many cell types like T cells, B cells, and epithelial cells after stimulation and activation by pro-inflammatory cytokines like IFN-γ and IL413.  \nFurthermore, PD1 cannot be expressed in rested T cells, and it is neutralized when engaged by PDL1 in the PD1-PDL1 axis in several ways including cytokine production with substantial efficacy on IFN-γ, IL2, and TNFα production14. Considering the important role of the PD1-PDL1 pathway in preventing autoimmunity in normal tissues, it is not wondering that PD1 axil has operated by tumor cells to escape from immune response  \n1Stem Cell Technology","cbCaisxmo22JlNZr","https://ap.wps.com/l/cbCaisxmo22JlNZr","pdf",3628607,18,"English","# Background: NSCLC and PD-1/PD-L1 immune evasion\n## Rationale for targeting PD-L1\n# Study objective and strategy\n## miR-138-5p targeting of CD274/PD-L1\n## Bioinformatics identification of miRNA–mRNA networks\n# Experimental approaches\n## Cell models and cytokine-stimulated conditions\n## Assessment of Jurkat survival and exhaustion\n# Findings and implications","[{\"question\":\"Why is the PD-1/PD-L1 pathway important in NSCLC immune evasion?\",\"answer\":\"PD-1 and PD-L1 act as co-inhibitory checkpoint molecules that tumors use to escape CD8+ T-cell killing. Their interaction promotes T-cell dysfunction, exhaustion, apoptosis, and reduced anti-tumor activity.\"},{\"question\":\"What role does miR-138-5p play in regulating PD-L1?\",\"answer\":\"The study evaluates miR-138-5p as a regulator that targets the CD274 (PD-L1) axis. By impairing PD-L1 expression, miR-138-5p is examined for effects on immune escape and downstream cellular responses.\"},{\"question\":\"How were Jurkat cells used to assess anti-tumor immunity effects?\",\"answer\":\"Jurkat cells and NSCLC cell lines were cultured under cytokine stimulation to model cancer environmental conditions. The experiments assess how miR-138-5p preserves Jurkat cell survival by modulating the PD-L1/PD-1 pathway and related exhaustion effects.\"}]","PDL1 targeting by miR-138-5p amplifies anti-tumor immunity and Jurkat cells survival in non-small cell lung cancer | PDF",1789996957,45]