The HDAC1 Knockout MCF-7 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MCF-7 human breast adenocarcinoma cell line. The engineered cells harbor a disruption of the HDAC1 gene, yielding a heterogeneous pool of loss-of-function mutants suitable for studying HDAC1-dependent processes. As a polyclonal population, the cells represent a diverse array of edited alleles, enabling robust and reproducible experimental outcomes without the clonal selection artifacts that may arise in single-cell-derived lines.
MCF-7 cells are estrogen receptor ?? (ER??)-positive, progesterone receptor (PR)-positive human breast epithelial adenocarcinoma cells with a luminal epithelial phenotype. Derived from a pleural effusion of metastatic breast adenocarcinoma, they are a widely used model for hormone-responsive breast cancer. Their hormone receptor expression and intact signaling pathways facilitate study of endocrine-regulated transcription and oncogenic mechanisms.
HDAC1 encodes a Class I histone deacetylase that deacetylates lysine residues primarily on histones H3 and H4, promoting chromatin compaction and transcriptional repression. Its activity is regulated by p53, E2F transcription factors, SP1, NF-??B, and MYC, and it is modulated by phosphorylation via CK2 and PKA. HDAC1 functions within Sin3, NuRD, and CoREST corepressor complexes, directly interacting with Sin3A, RbAp46/48, LSD1, and MTA1/2. Beyond histones, it deacetylates non-histone substrates including p53, E2F1, STAT3, and ??-tubulin, thereby influencing cell cycle progression, apoptosis, and signal transduction. A critical downstream consequence is the transcriptional repression of the tumor suppressor CDKN1A (p21/WAF1).
In MCF-7 cells, HDAC1 knockout results in histone hyperacetylation, chromatin relaxation, and derepression of tumor-suppressor genes including CDKN1A. This impairs cell cycle progression, reduces proliferation, and may sensitize cells to endocrine therapies or DNA-damaging agents. Given HDAC1??s interaction with estrogen receptor signaling, the model is particularly relevant for dissecting epigenetic contributions to hormone receptor-positive breast cancer and resistance mechanisms.
Key applications encompass functional studies of HDAC1 in breast cancer, investigation of epigenetic gene regulation, and HDAC inhibitor screening. Assays include Western blotting for HDAC1 and acetylated histones, RT-qPCR for p21 and ER??, ChIP-qPCR for histone acetylation, cell proliferation assays (MTT, colony formation), flow cytometry for cell cycle, apoptosis assays (Annexin V), migration/invasion studies, and drug sensitivity testing with compounds like Vorinostat. This polyclonal knockout resource supports drug discovery and mechanistic exploration. For further information, contact Ascent Research.
