The HCFC1R1 Knockout T-47D Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in the T-47D human breast carcinoma line. Targeted disruption of HCFC1R1 provides a loss-of-function model to study transcriptional control and cell cycle regulation. As a polyclonal pool, these cells preserve heterogeneous knockout events, offering a genetically representative background without clonal artifacts. The knockout is achieved via CRISPR/Cas9-mediated gene disruption, enabling dissection of HCFC1R1 in breast cancer and viral-host interactions.
T-47D is an ER+, PR+, and androgen receptor-positive breast carcinoma cell line with luminal epithelial characteristics. Isolated from pleural effusion of a 54-year-old female with infiltrating ductal carcinoma, it is a well-established model for hormone-dependent breast cancer. The line recapitulates estrogen-dependent growth and sensitivity to hormone therapies like tamoxifen, making it ideal for studying signaling and cell cycle crosstalk.
HCFC1R1 acts as a negative regulator of the transcriptional coactivator HCFC1. Knockout derepresses HCFC1, leading to enhanced E2F target gene transcription (e.g., CCNE1, CDK2) that drives G1/S transition and proliferation. It also modulates Oct-1-dependent expression, affecting herpes simplex virus replication via VP16. The regulatory network includes upstream E2F1, HCFC1, and ESR1, with downstream effectors like the Set1/COMPASS complex linking transcription to chromatin modification. Direct interaction with HCFC1 places HCFC1R1 at the nexus of cell cycle, hormone signaling, and viral gene expression.
In T-47D cells, HCFC1R1 disruption is predicted to promote proliferation and alter hormone signaling due to E2F and estrogen receptor pathway involvement. This model enables dissection of HCFC1R1??s tumor-suppressive role and its impact on HCFC1-mediated networks. It provides a system to study loss of HCFC1R1 effects on cell cycle progression, estrogen-dependent growth, and drug response. The interplay with viral transactivators also makes it valuable for host-factor studies in HSV infection.
This polyclonal knockout pool supports functional genomics, drug sensitivity screening, and mechanistic studies. Applications include flow cytometry for cell cycle, RT-qPCR for E2F targets, and Western blotting. It aids in hormone therapy resistance studies with tamoxifen or CDK4/6 inhibitors like palbociclib, assessed by proliferation and colony formation assays. ChIP-qPCR can evaluate H3K4me3 changes downstream of Set1/COMPASS. Viral assays dissect HCFC1R1??s role in HSV replication, while RNA-seq enables transcriptomic profiling. For additional details, contact Ascent Research.
