ArticleIn vivo (Athens, Greece)
Role of EMP2 and Del-1 in Tamoxifen-resistant Breast Cancer Cells.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND/
aimEndocrine resistance remains a major clinical challenge in hormone receptor-positive (HR+) breast cancer. Although developmental endothelial locus-1 (Del-1) has been implicated in endocrine resistance, the regulatory pathways interacting with Del-1 remain poorly defined. This study aimed to identify molecular components associated with Del-1-driven resistance by performing RNA sequencing in tamoxifen-resistant (TAMR) breast cancer cells following Del-1 knockdown. MATERIALS AND
methodsRNA sequencing was conducted in TAMR MCF-7 cells following Del-1 silencing to identify Del-1-regulated pathways in endocrine-resistant disease. Among the genes up-regulated after Del-1 suppression, epithelial membrane protein 2 (EMP2) was selected for further investigation due to its reported roles in cellular adhesion, metabolic signaling, and cancer stemness. Gene expression changes were validated using reverse transcription polymerase chain reaction (RT-PCR). Functional studies were performed using small interfering RNA (siRNA)-mediated knockdown of EMP2 or Del-1, followed by proliferation and clonogenic assays.
resultsBoth EMP2 and Del-1 were up-regulated in luminal breast cancer cell lines. Suppression of Del-1 increased EMP2 expression in TAMR cells, consistent with RNA-seq findings. Notably, EMP2 suppression resulted in an increase in Del-1 expression, suggesting a potential regulatory feedback loop. Furthermore, knockdown of either Del-1 or EMP2 substantially enhanced colony formation in TAMR cells compared with controls.
conclusionEMP2 may be involved in the regulation of Del-1 expression in TAMR breast cancer cells. Modulation of Del-1 or EMP2 influences cancer stemness in TAMR cells, underscoring the Del-1-EMP2 axis as a potential therapeutic target to overcome endocrine resistance.
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