The IGF2BP3 Knockout T-47D Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population of T-47D breast cancer cells in which the IGF2BP3 gene has been disrupted. This heterogeneous knockout pool allows functional investigation of IGF2BP3 without the clonal selection biases of single-cell-derived lines, and retains genetic diversity while uniformly ablating target gene function.
T-47D cells are a well-characterized human breast cancer line derived from a pleural effusion of a ductal carcinoma. They are estrogen receptor-positive, progesterone receptor-positive, and androgen receptor-positive, and are widely used as a model of luminal A breast cancer, retaining hormone-responsive growth and representing a clinically relevant system for studying endocrine signaling crosstalk with post-transcriptional networks.
IGF2BP3 encodes an oncofetal RNA-binding protein that stabilizes and regulates translation of oncogenic mRNAs. It is activated by upstream factors including HMGA2, MYC, ??-catenin, LIN28B, IGF1, and EGF, and directly binds and stabilizes transcripts such as MYC, CD44, HMGA2, KRAS, CCND1, VIM, and SNAI1. Through interactions with IGF2BP1, IGF2BP2, ELAVL1/HuR, EIF4E, and MATR3, IGF2BP3 enhances translation efficiency, amplifying signaling via the IGF1R-PI3K-AKT-mTOR and MAPK/ERK cascades, thereby driving cell proliferation, migration, and epithelial-mesenchymal transition (EMT). Disruption of IGF2BP3 in T-47D cells abolishes this stabilization, impairing downstream pathway outputs and reducing oncogenic phenotypes.
In the T-47D hormonal context, IGF2BP3 knockout is expected to disrupt estrogen- and growth-factor-driven proliferative signaling, as IGF2BP3 lies downstream of the IGF1 receptor and EGF receptor pathways. Reduced expression of cyclin D1 (CCND1) and anti-apoptotic BCL2 may sensitize cells to apoptosis, while diminished VIM and SNAI1 levels suppress EMT-like phenotypes. This model thus facilitates detailed dissection of RNA-binding protein contributions to hormone receptor-positive breast cancer progression, metastasis, and the development of endocrine therapy resistance.
This polyclonal knockout pool supports a broad range of applications, including investigation of mRNA stability and translation control via RT-qPCR and RNA immunoprecipitation sequencing (RIP-seq), transcriptome-wide analysis by RNA-seq, and functional assays such as western blotting, cell proliferation, migration, invasion, apoptosis, immunofluorescence, and phospho-signaling arrays. It provides a powerful system for studying oncogenic RNA-binding proteins, validating IGF2BP3 as a therapeutic target, and exploring crosstalk between growth factor and hormone signaling pathways. For technical information and ordering details, contact Ascent Research.
