Posters
Presenting Author Academic/Professional Position
Undergraduate
Academic Level (Author 1)
Undergraduate
Discipline/Specialty (Author 1)
Immunology and Microbiology
Academic Level (Author 2)
Post-doc
Discipline/Specialty (Author 2)
Immunology and Microbiology
Academic Level (Author 3)
Graduate Student
Discipline/Specialty (Author 3)
Immunology and Microbiology
Academic Level (Author 4)
Post-doc
Discipline/Specialty (Author 4)
Immunology and Microbiology
Academic Level (Author 5)
Undergraduate
Discipline/Specialty (Author 5)
Immunology and Microbiology
Presentation Type
Poster
Discipline Track
Biomedical Science
Abstract Type
Research/Clinical
Abstract
Background: The G protein–coupled estrogen receptor (GPER) mediates rapid non-genomic estrogen signaling and has been implicated in breast cancer progression and aggressiveness. However, its expression patterns across molecular subtypes and its direct functional contribution to tumor behavior remain incompletely defined. The objective of this study was to comprehensively characterize GPER expression in breast cancer tissues and to functionally validate its role in regulating tumor cell proliferation and migration using genetic modulation approaches.
Methods: GPER expression was evaluated in breast cancer cell lines and patient tumor tissues using immunohistochemistry (IHC), Western blotting, and RT-PCR. Tumors were classified into Luminal A, Luminal B, HER2-enriched, and triple-negative subtypes. GPER expression and subcellular localization (cytoplasmic and nuclear) were analyzed in relation to metastatic status, tumor grade, histological grade, tumor location within the breast, age, ethnicity, and body mass index (BMI). For functional validation, HCC1937 triple-negative breast cancer cells were engineered to overexpress GPER (GPER-OE) or undergo CRISPR-Cas9–mediated knockdown using sgRNA constructs, with GPER-V serving as a control. GPER modulation was confirmed by Western blot and qPCR. Cell viability was assessed using live/dead assays, clonogenic potential by colony formation assays, and cell migration by wound healing assays. Proteomic profiling was performed on transduced cell lines to identify GPER-associated signaling changes. Statistical analyses included correlation testing and subgroup comparisons.
Results: GPER was broadly expressed across all breast cancer subtypes at both the protein and mRNA levels. IHC revealed variable cytoplasmic and nuclear localization, with higher expression in metastatic compared to non-metastatic tumors. GPER expression differed significantly by molecular subtype and was associated with tumor grade, histological grade, tumor location, age, ethnicity, and BMI. Western blot and RT-PCR confirmed subtype-dependent differences in GPER abundance. In functional studies, GPER overexpression significantly increased cell viability, colony formation, and wound closure, whereas CRISPR-mediated GPER knockdown produced the opposite effects. Proteomic analysis revealed distinct signaling profiles associated with GPER modulation, supporting a direct role for GPER in regulating aggressive tumor phenotypes.
Conclusions: GPER is widely expressed in breast cancer and demonstrates strong associations with clinicopathologic features and tumor aggressiveness. Genetic modulation experiments confirm that GPER directly promotes proliferative and migratory phenotypes, establishing GPER as a biologically significant driver of breast cancer progression.
Recommended Citation
Vidaurri, Sierra E.; Singh, Shweta; Ledezma, Valerie E.; Baru, Rajasekhar; Garza, Emma; Flores, Francisco; Noorani, Muhammad; Goyal, Shubhank; Calderon, Aura; Lim, Alexander; Dhasmana, Anupam; Dhasmana, Swati; Yallapu, Murali; Chauhan, Subhash; Nguyen, Diane; and Khan, Sheema, "Expression and Functional Significance of the G Protein–Coupled Estrogen Receptor (GPER) in Breast Cancer Subtypes" (2026). Research Symposium. 6.
https://scholarworks.utrgv.edu/somrs/2026/posters/6
Included in
Expression and Functional Significance of the G Protein–Coupled Estrogen Receptor (GPER) in Breast Cancer Subtypes
Background: The G protein–coupled estrogen receptor (GPER) mediates rapid non-genomic estrogen signaling and has been implicated in breast cancer progression and aggressiveness. However, its expression patterns across molecular subtypes and its direct functional contribution to tumor behavior remain incompletely defined. The objective of this study was to comprehensively characterize GPER expression in breast cancer tissues and to functionally validate its role in regulating tumor cell proliferation and migration using genetic modulation approaches.
Methods: GPER expression was evaluated in breast cancer cell lines and patient tumor tissues using immunohistochemistry (IHC), Western blotting, and RT-PCR. Tumors were classified into Luminal A, Luminal B, HER2-enriched, and triple-negative subtypes. GPER expression and subcellular localization (cytoplasmic and nuclear) were analyzed in relation to metastatic status, tumor grade, histological grade, tumor location within the breast, age, ethnicity, and body mass index (BMI). For functional validation, HCC1937 triple-negative breast cancer cells were engineered to overexpress GPER (GPER-OE) or undergo CRISPR-Cas9–mediated knockdown using sgRNA constructs, with GPER-V serving as a control. GPER modulation was confirmed by Western blot and qPCR. Cell viability was assessed using live/dead assays, clonogenic potential by colony formation assays, and cell migration by wound healing assays. Proteomic profiling was performed on transduced cell lines to identify GPER-associated signaling changes. Statistical analyses included correlation testing and subgroup comparisons.
Results: GPER was broadly expressed across all breast cancer subtypes at both the protein and mRNA levels. IHC revealed variable cytoplasmic and nuclear localization, with higher expression in metastatic compared to non-metastatic tumors. GPER expression differed significantly by molecular subtype and was associated with tumor grade, histological grade, tumor location, age, ethnicity, and BMI. Western blot and RT-PCR confirmed subtype-dependent differences in GPER abundance. In functional studies, GPER overexpression significantly increased cell viability, colony formation, and wound closure, whereas CRISPR-mediated GPER knockdown produced the opposite effects. Proteomic analysis revealed distinct signaling profiles associated with GPER modulation, supporting a direct role for GPER in regulating aggressive tumor phenotypes.
Conclusions: GPER is widely expressed in breast cancer and demonstrates strong associations with clinicopathologic features and tumor aggressiveness. Genetic modulation experiments confirm that GPER directly promotes proliferative and migratory phenotypes, establishing GPER as a biologically significant driver of breast cancer progression.
