{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T05:28:36Z","timestamp":1786512516243,"version":"build-2736575974"},"reference-count":54,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T00:00:00Z","timestamp":1786492800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Obesity-associated alterations in the tumor microenvironment (TME) modulate breast cancer (BC) progression. In obese individuals, adipocytes, the predominant stromal component of breast tissue, display an altered endocrine and inflammatory profile, leading to increased secretion of hormones, adipokines, and cytokines that influence epithelial cell behavior and contribute to tumor progression and therapeutic resistance. In the metastatic setting, antibody\u2013drug conjugates (ADCs) have expanded the therapeutic landscape of BC. However, resistance remains a clinical challenge, with loss or downregulation of the target antigen representing a key mechanism. Increasing evidence indicates that TME-derived signals regulate therapeutic target expression. Among these, Trophoblast Cell Surface Antigen 2 (TROP2), a clinically validated ADC target, can be modulated by stromal-derived factors Here, we investigated whether adipocytes regulate TROP2 expression and influence the efficacy of TROP2-directed ADCs in BC cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Conditioned media (CM) from differentiated 3T3-L1 adipocytes were applied to ER\u03b1-positive (MCF-7, T47D) and ER\u03b1-negative (MDA-MB-231) BC cells. TROP2 expression was evaluated by qRT-PCR and immunoblotting. Estradiol levels in adipocyte CM were quantified by ELISA, and ER\u03b1 signaling was inhibited using tamoxifen and fulvestrant. In silico analyses assessed the relationship between ER\u03b1 signaling and TACSTD2 expression and evaluated TACSTD2 levels in BC cohorts stratified by body mass index (BMI). Cell viability assays determined responsiveness to Sacituzumab Govitecan and Datopotamab Deruxtecan.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Adipocyte-derived CM significantly reduced TROP2 expression at transcript and protein levels, selectively in ER\u03b1-positive BC models. Elevated 17\u03b2-estradiol levels were detected in adipocyte CM, and estradiol exposure recapitulated TROP2 downregulation. Pharmacological inhibition of ER\u03b1 signaling or the blockade of estrogen production abrogated this effect, supporting a role for ER\u03b1 activation. In silico analyses suggested a functional link between ER\u03b1 and TROP2. TROP2 expression was reduced in tumors from overweight\/obese patients with ER\u03b1-positive BC, but not in ER\u03b1-negative cases. Functionally, adipocyte CM counteracted the antiproliferative effects of Sacituzumab Govitecan and Datopotamab Deruxtecan in ER\u03b1-positive BC cells, an effect that was reversed by ER\u03b1 inhibition.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings identify an estrogen-dependent, adipocyte-driven mechanism that modulates TROP2 expression and reduces responsiveness to TROP2-directed ADCs in ER\u03b1-positive BC models. Our data highlight the contribution of obesity-associated adipose tissue dysfunction to variability in targeted therapy response and warrant further investigation in clinically relevant settings.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fendo.2026.1866290","type":"journal-article","created":{"date-parts":[[2026,8,12]],"date-time":"2026-08-12T04:46:45Z","timestamp":1786510005000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Adipocyte-derived estrogen signaling influences TROP2 expression in ER\u03b1-positive breast cancer"],"prefix":"10.3389","volume":"17","author":[{"given":"Luca","family":"Gelsomino","sequence":"first","affiliation":[{"name":"Department of Pharmacy, Health and Nutritional Sciences, University of Calabria","place":["Cosenza, Italy"]},{"name":"Centro Sanitario, University of Calabria","place":["Cosenza, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda","family":"Manna","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Health and Nutritional Sciences, University of Calabria","place":["Cosenza, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vittoria","family":"Marchio","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Health and Nutritional Sciences, University of Calabria","place":["Cosenza, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Piercarlo","family":"Del Console","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Health and Nutritional Sciences, University of Calabria","place":["Cosenza, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giuseppina","family":"Augimeri","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Health and Nutritional Sciences, University of Calabria","place":["Cosenza, Italy"]},{"name":"Centro Sanitario, University of Calabria","place":["Cosenza, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cinzia","family":"Giordano","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Health and Nutritional Sciences, University of Calabria","place":["Cosenza, Italy"]},{"name":"Centro Sanitario, University of Calabria","place":["Cosenza, Italy"]},{"name":"Clinical Laboratory Unit, Azienda Ospedaliera (AO) \u201cAnnunziata\u201d","place":["Cosenza, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bal\u00e1zs","family":"Gy\u0151rffy","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics, Semmelweis University","place":["Budapest, Hungary"]},{"name":"Institute of Transdisciplinary Discoveries, Medical School, University of Pecs","place":["Pecs, Hungary"]},{"name":"Cancer Biomarker Research Group, Institute of Molecular Life Sciences, Hungarian Research Network","place":["Budapest, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniela","family":"Bonofiglio","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Health and Nutritional Sciences, University of Calabria","place":["Cosenza, Italy"]},{"name":"Centro Sanitario, University of Calabria","place":["Cosenza, Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carmine","family":"De Angelis","sequence":"additional","affiliation":[{"name":"Clinical and Translational Oncology, Scuola Superiore","place":["Naples, Italy"]},{"name":"National Cancer Institute, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Fondazione G. 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