The KRCC1 Knockout HT29 Polyclonal Cells product is a heterogeneous population of HT29 colorectal adenocarcinoma cells engineered with CRISPR/Cas9-mediated disruption of the KRCC1 gene, generating a loss-of-function model for investigating the role of this lysine-rich coiled-coil protein in cancer biology. This polyclonal knockout cell population enables pooled analysis of gene function without clonal selection, offering a representative range of editing outcomes across the cell population.
The HT29 host cell line is a widely used epithelial model derived from a primary colorectal adenocarcinoma of a 44-year-old female Caucasian. These cells exhibit an adherent epithelial morphology and are extensively employed for studying intestinal epithelial physiology, mucin production, and mechanisms of colorectal carcinogenesis. The HT29 line provides a well-characterized background for examining oncogenic signaling, drug responses, and the molecular basis of colorectal tumor progression.
KRCC1 is a multidomain adaptor protein that promotes cell proliferation, migration, and invasion through activation of the PI3K/AKT and MAPK/ERK signaling cascades. The protein is regulated transcriptionally by c-Myc and post-transcriptionally by miR-30a-5p, and it responds to EGF/EGFR stimulation. Downstream, KRCC1 enhances phosphorylation of AKT and its effectors mTOR and p70S6K, leading to increased expression of Cyclin D1, MMP9, and the anti-apoptotic factor BCL2. Concurrently, it engages the Ras-Raf-MEK-ERK axis to drive cell cycle progression and motility. KRCC1 interacts with the p85 regulatory subunit of PI3K and with AKT, and its coiled-coil domains are predicted to mediate interactions with cytoskeletal components, reinforcing its role in focal adhesion and actin dynamics.
In the context of HT29 colorectal adenocarcinoma cells, abrogating KRCC1 function provides a powerful tool to dissect its contributions to malignant phenotypes. These cells inherently harbor mutations in APC, TP53, and other colorectal cancer driver genes, making the KRCC1 knockout a relevant model for studying additive or synergistic effects on tumor growth and resistance. This model can be used to assess the impact of KRCC1 loss on PI3K/AKT and MAPK/ERK pathway activity, cell cycle progression, and apoptosis regulation, particularly in relation to chemotherapeutic sensitivity. The interplay between KRCC1 and miR-30a-5p can also be investigated in this system, offering insights into post-transcriptional control mechanisms in colorectal cancer.
The KRCC1 Knockout HT29 Polyclonal Cells are suitable for a wide range of cancer biology applications, including proliferation assays using MTT or CCK-8, migration and invasion studies via Transwell assays, and flow cytometric analysis of apoptosis and cell cycle distribution. They enable phospho-specific analysis of PI3K/AKT/mTOR pathway components by Western blotting and RT-qPCR validation of downstream target genes. Additionally, these cells serve as a platform for drug sensitivity screening to identify chemosensitizing agents and for functional validation of miR-30a-5p-mediated regulation. For detailed product information or technical support, please contact Ascent Research.
