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This study evaluates somatostatin receptor 2 (SSTR2) as an imaging/therapy target and tests whether histone deacetylase (HDAC) inhibition can induce SSTR2 expression. Mouse samples were analyzed by Western blot, immunohistochemistry, qRT-PCR, flow cytometry, and cell binding assays. [68Ga]Ga-DOTATATE PET characterized SSTR2 in EO771 and 4T1 models before and after HDAC inhibition, showing upregulation at transcriptional, translational, and functional levels.",{"@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/characterizing-sstr2-expression-and-modulation-for-targeted-imaging-and-therapy-in-preclinical-models-of-triple-negative-breast-cancer/371341/",{"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/characterizing-sstr2-expression-and-modulation-for-targeted-imaging-and-therapy-in-preclinical-models-of-triple-negative-breast-cancer/371341.png","ImageObject",300,407,{"name":92,"@type":93},"Riley","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-28","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":44},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"Why focus on SSTR2 in triple-negative breast cancer?","Question",{"text":112,"@type":113},"SSTR2 can be overexpressed in some cancers while remaining low in normal tissues, making it a candidate for targeted imaging and therapy. The study highlights SSTR2 as a promising molecular target in TNBC.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does the study test whether HDAC inhibitors modulate SSTR2?",{"text":117,"@type":113},"SSTR2 basal expression and induction after HDAC inhibition are evaluated using Western blot, immunohistochemistry, qRT-PCR, flow cytometry, and cell binding assays. These assess changes at multiple biological levels.",{"name":119,"@type":110,"acceptedAnswer":120},"How is SSTR2 assessed non-invasively in the TNBC models?",{"text":121,"@type":113},"The study uses [68Ga]Ga-DOTATATE PET imaging, which targets SSTR2, to characterize expression and its variability in EO771 and 4T1 models before and after HDAC inhibition.","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},371341,1790258459,{"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":44,"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":41},1374391975076,"https://ap-avatar.wpscdn.com/avatar/14000253ca4ec9f6853?x-image-process=image/resize,m_fixed,w_180,h_180&k=1783305029341752051","[www. nature.com/scientificreports](www. nature.com/scientificreports)  \nOPEN  \nCharacterizing SSTR2 expression and modulation for targeted imaging and therapy in preclinical models of triple-negative breast cancer  \nShannon E. Lynch1,2, Corinne I. Crawford1,5, Hailey A. Houson1, James M. Omweri3, Piyasuda Pukkanasut3, Carlos A. Gallegos1,5, Jason D. Whitt4, Renata Jaskula-Sztul4,6, Suzanne E. Lapi1,3,6 & Anna G. Sorace1,5,6􀀍  \nPatients with breast cancer which lack molecular targets, such as human epidermal growth factor receptor 2 (HER2) or hormone receptors, have limited access to targeted therapies. Somatostatin receptor 2 (SSTR2) is overexpressed in some cancers, and SSTR2-targeted radiopharmaceuticals are FDA-approved fortheranostic targeted imaging and therapy in neuroendocrine tumors (NETs) . Importantly, histone deacetylase (HDAC) inhibitors can epigenetically modulate SSTR2 expression in NETs with low or variable basal expression. The goal of this study is to characterize SSTR2 basal expression and induction via HDAC inhibition as a potential target for imaging and therapy in preclinical models of triple-negative breast cancer (TNBC) . SSTR2 expression in mouse samples was assessed via Western blot and immunohistochemistry. Real-time quantitative PCR (qRT-PCR), flow cytometry, and cell binding assays were utilized to determine if HDAC inhibition can upregulate SSTR2 expression. [ 68Ga]Ga-DOTATATE positron emission tomography (PET) imaging, which targets SSTR2, was used to non-invasively characterize SSTR2 expression and variability in the EO771 and 4T1 TNBC models before and after HDAC inhibition. These studies demonstrate that HDAC inhibition can upregulate SSTR2 at the transcriptional, translational, and functional levels in breast cancer. Importantly, SSTR2 expression can be characterized non-invasively via PET imaging and modulation with HDAC inhibitors can be monitored longitudinally. Our findings highlight SSTR2 as a promising therapeutic molecular target inTNBC.  \nKeywords PET, Breast cancer, SSTR2, SAHA, HDAC, Preclinical  \nBreast cancer (BC) is the most common female cancer globally, with 10–20% of those cases being triplenegative1,2. TNBC, an aggressive and highly heterogeneous subtype of BC, is characterized by the absence of molecular targets found in other subtypes of BC including estrogen receptor (ER), progesterone receptor (PR), and HER23,4. Due to the lack of therapeutic targets, there are currently no approved targeted therapies for patients with TNBC4–6. Current standard-of-care treatments have improved survival but are only effective in a small percentage of patients7–9. Therefore, identifying novel, targetable biomarkers in breast cancer are of interest.  \nSomatostatin receptors are overexpressed in some cancer tissues and there are clinically approved theranostic agents available for NETs. SSTR2 is a good potential molecular target for imaging and therapy due to its low expression in normal tissues10, 11. PET imaging can non-invasively inform on molecular signatures within tumors, creating biomarkers of response or characterizing targets for therapy. Importantly, we can obtain  \n1Department of Radiology, The University of Alabama at Birmingham, VH G082, 1670 University Blvd, Birmingham, AL 35233, USA. 2Graduate Biomedical Sciences, The University of Alabama at Birmingham, Birmingham, AL, USA.  \n3Department of Chemistry, The University of Alabama at Birmingham, Birmingham, AL, USA. 4Department of Surgery, The University of Alabama at Birmingham, Birmingham, AL, USA. 5Department of Biomedical Engineering, The University of Alabama at Birmingham, Birmingham, AL, USA. 6O’Neal Comprehensive Cancer Center, The University of Alabama at Birmingham, Birmingham, AL, USA. 􀀍 email: [asorace@uabmc.edu](asorace@uabmc.edu)  \n[www. nature.com/scientificreports/](www. nature.com/scientificreports/)  \nquantitative metrics about underlying tumor biology to characterize tumors including glucose metabolism, cell pro","cbCaiurHS4NRKsca","https://ap.wps.com/l/cbCaiurHS4NRKsca","pdf",3616888,12,"English","# Background and rationale\n## Triple-negative breast cancer and lack of targeted therapies\n## SSTR2 as a theranostic target\n# Experimental approach\n## Assessing SSTR2 expression in mouse samples\n## Measuring functional upregulation after HDAC inhibition\n## Non-invasive PET imaging with [68Ga]Ga-DOTATATE\n# Study aims and implications","[{\"question\":\"Why focus on SSTR2 in triple-negative breast cancer?\",\"answer\":\"SSTR2 can be overexpressed in some cancers while remaining low in normal tissues, making it a candidate for targeted imaging and therapy. The study highlights SSTR2 as a promising molecular target in TNBC.\"},{\"question\":\"How does the study test whether HDAC inhibitors modulate SSTR2?\",\"answer\":\"SSTR2 basal expression and induction after HDAC inhibition are evaluated using Western blot, immunohistochemistry, qRT-PCR, flow cytometry, and cell binding assays. These assess changes at multiple biological levels.\"},{\"question\":\"How is SSTR2 assessed non-invasively in the TNBC models?\",\"answer\":\"The study uses [68Ga]Ga-DOTATATE PET imaging, which targets SSTR2, to characterize expression and its variability in EO771 and 4T1 models before and after HDAC inhibition.\"}]","Characterizing SSTR2 expression and modulation for targeted imaging and therapy in preclinical models of triple-negative breast cancer | PDF",1790191850]