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This study investigated how the Sam pointed domain-containing ETS transcription factor (SPDEF) influences PAAD progression. Differential gene analysis using TCGA highlighted SPDEF as a key PAAD gene, and Kaplan–Meier analysis supported its prognostic relevance. Cell-based experiments confirmed SPDEF regulation of proliferation, apoptosis, migration, and invasion, including effects on mRNA and protein levels. Mechanistically, SPDEF increased S100A16 transcription and promoted malignant phenotypes via PI3K/AKT pathway activation, identifying therapeutic targets within SPDEF-driven signaling.",{"@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/spdef-drives-pancreatic-adenocarcinoma-progression-via-transcriptional-upregulation-of-s100a16-and-activation-of-the-pi3kakt-signaling-pathway/328801/",{"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/spdef-drives-pancreatic-adenocarcinoma-progression-via-transcriptional-upregulation-of-s100a16-and-activation-of-the-pi3kakt-signaling-pathway/328801.png","ImageObject",300,407,{"name":92,"@type":93},"Levi","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-26","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":24},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What was the main purpose of this study on SPDEF in pancreatic adenocarcinoma?","Question",{"text":112,"@type":113},"To elucidate the molecular mechanisms by which SPDEF impacts pancreatic adenocarcinoma progression.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How did the study evaluate SPDEF’s prognostic significance?",{"text":117,"@type":113},"It used TCGA-based analysis of differentially expressed genes and performed Kaplan–Meier survival analysis to assess prognostic relevance.",{"name":119,"@type":110,"acceptedAnswer":120},"What mechanism links SPDEF to pancreatic cancer progression?",{"text":121,"@type":113},"SPDEF enhances transcription of S100A16, and this promotes cell migration, proliferation, and invasion by activating the PI3K/AKT signaling pathway.","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},328801,1790164113,{"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":24,"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,"preview_page_count":4},7971461740909,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","RESEARCH ARTICLE  \nSPDEF drives pancreatic adenocarcinoma progression via transcriptional upregulation ofS100A16 and activation of the PI3K/AKT signaling pathway  \nHang Jiang 1\\#, Zhiqian Xue 1\\#, Liping Zhao 1\\#, Boyuan Wang 2, Chenfei Wang 3 ∗ , Haihan Song 1 , 4, 5 ∗ , and Jianjun Sun 1 ∗  \nPancreatic adenocarcinoma (PAAD) is a notably aggressive malignancy with limited treatment options and an unfavorable prognosis for patients. The objective of this study was to elucidate the molecular mechanisms by which Sam pointed domain-containing ETS transcription factor (SPDEF) impacts PAAD progression. Analysis of differentially expressed genes (DEGs) and their association with ETS family members, conducted through The Cancer Genome Atlas (TCGA) database, identified SPDEF as a key gene within the molecular framework of PAAD. Kaplan-Meier (KM) survival analysis highlighted the prognostic relevance of SPDEF. In vitro experiments validated the association with cell proliferation and apoptosis, affecting pancreatic cancer cell dynamics. Elevated SPDEF expression was observed in PAAD tumor samples, further establishing its role in this disease. Our in vitro assays revealed that SPDEF regulates mRNA and protein expression levels, significantly affecting cell proliferation. Moreover, an association was established between SPDEF and a reduction in apoptosis, alongside an increase in cell migration and invasion. An in-depth analysis of  \nSPDEF-targeted genes revealed four crucial genes for the advanced prognostic model, among which S100A16 was significantly correlated with SPDEF. Mechanistic analysis showed that SPDEF enhances the transcription ofS100A16, which in turn enhances PAAD cell migration, proliferation, and invasion by activating the PI3K/AKT signaling pathway. Our study revealed the critical role of SPDEF in promoting PAAD by upregulating S100A16 transcription and stimulating the PI3K/AKT signaling pathway, thereby deepening the understanding of the molecular evolution of pancreatic cancer and revealing new therapeutic targets in the SPDEF-driven pathways.  \nKeywords: Pancreatic adenocarcinoma (PAAD), Sam pointed domain-containing ETS transcription factor (SPDEF), S100A16, PI3K/AKT signaling pathway.  \nIntroduction  \nThe global prevalence of pancreatic adenocarcinoma (PAAD) has rapidly increased, highlighting the critical importance of early detection and timely intervention [1, 2] . Due to its insidious nature and the lack of distinctive early symptoms, diagnosis is often delayed, resulting in advanced stages of the disease that are frequently inoperable [3, 4] . Late detection of PAAD complicates treatment and reduces the likelihood of a positive outcome for the patient duetothe aggressive progression of the cancer. Furthermore, the inherent resistance of PAAD to several conventional treatments means that even if diagnosed early, the treatment effectiveness may still be limited [5] . The genetic heterogeneity of PAAD suggests that tailored treatment options maybe more effectivethan universal strategies [6, 7]. Advancements in personalized medicine and genomic profiling offer promising avenues in this realm. By recognizing the specific genetic aberrations and molecular mechanisms of individual  \ntumors may enable clinicians to design more precise and effective therapeutic interventions.  \nThe PI3K/AKT signaling pathway is crucial for cellular homeostasis and growth. However, when dysregulated, it can contribute to various diseases, particularly cancer [8, 9] . Its role in PAAD is highlighted by a complex network of signaling cascades, feedback mechanisms, and interactions with other pathways, collectively influencing the progression of cancer cells [10, 11]. Aberrant activation of the PI3K/AKT pathway provides a proliferative edge to pancreatic tumor cells [12] . This signaling pathway promotes unchecked cell proliferation, circumvents apoptotic processes, and stimulates angiogenesis, all of which are crucial for tumor survival [13, 14","cbCaieryKlb4VPwk","https://ap.wps.com/l/cbCaieryKlb4VPwk","pdf",3610132,13,"English","# Introduction\n## Pancreatic adenocarcinoma burden and diagnosis challenges\n## PI3K/AKT signaling pathway in cancer progression","[{\"question\":\"What was the main purpose of this study on SPDEF in pancreatic adenocarcinoma?\",\"answer\":\"To elucidate the molecular mechanisms by which SPDEF impacts pancreatic adenocarcinoma progression.\"},{\"question\":\"How did the study evaluate SPDEF’s prognostic significance?\",\"answer\":\"It used TCGA-based analysis of differentially expressed genes and performed Kaplan–Meier survival analysis to assess prognostic relevance.\"},{\"question\":\"What mechanism links SPDEF to pancreatic cancer progression?\",\"answer\":\"SPDEF enhances transcription of S100A16, and this promotes cell migration, proliferation, and invasion by activating the PI3K/AKT signaling pathway.\"}]","SPDEF drives pancreatic adenocarcinoma progression via transcriptional upregulation of S100A16 and activation of the PI3K/AKT signaling pathway | PDF",1789981070,33]