The GPER1 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 143B osteosarcoma cell line, in which the G protein-coupled estrogen receptor 1 (GPER1) gene has been disrupted to create a loss-of-function model. This polyclonal population contains a heterogeneous mixture of edited alleles, enabling the study of GPER1 deficiency without clonal selection artifacts. The cell product provides a reliable tool for investigating GPER1-mediated signaling pathways and their roles in cancer biology and drug response.
The 143B cell line is a thymidine kinase?Cnegative derivative of the HOS human osteosarcoma line, characterized by high metastatic potential and widely used as a model for osteosarcoma progression and bone metastasis. These cells exhibit aggressive growth properties and are commonly employed in both in vitro and in vivo assays to dissect mechanisms of tumor invasion, migration, and therapeutic resistance. The 143B host provides a clinically relevant context for examining the contributions of estrogen receptor signaling to bone cancer pathogenesis.
GPER1 is a seven-transmembrane G protein-coupled estrogen receptor that mediates rapid, non-genomic estrogenic responses. Upon activation by ligands such as 17??-estradiol or the selective agonist G-1, GPER1 couples to G??i and G??s proteins, leading to stimulation of adenylyl cyclase and phospholipase C, thereby elevating intracellular cAMP and calcium levels. These second messengers trigger downstream kinase cascades including the MAPK/ERK pathway via Src-Ras-Raf-MEK-ERK1/2 and the PI3K/Akt pathway, promoting cell proliferation, survival, and migration. GPER1 signaling also involves ??-arrestin?Cmediated scaffolding, cross-talk with EGFR, and transcriptional regulation of cyclin D1, MMP-9, and VEGF.
In the 143B osteosarcoma background, GPER1 knockout disrupts estrogen-driven oncogenic signaling, potentially attenuating metastatic traits and sensitizing cells to therapeutic interventions. Given that GPER1 is implicated in the progression of breast, ovarian, and endometrial cancers, as well as in osteoporosis and cardiovascular disease, this knockout model allows for dissecting the receptor??s specific contributions to bone?tumor microenvironments and hormone?responsive pathways. The polyclonal nature of the knockout population avoids biases associated with single?cell clones and better reflects the genetic heterogeneity observed in tumor specimens.
Researchers can employ these cells for western blotting, RT?qPCR, immunofluorescence, and functional assays such as calcium flux, cAMP measurement, and ERK phosphorylation analysis following estrogen stimulation. Additional applications include proliferation, migration, invasion, colony formation, apoptosis, and RNA?seq profiling. These knockout cells are valuable for drug sensitivity studies and target validation in osteosarcoma. For more information or custom services, contact Ascent Research.
