The ACP1 Knockout HCT 116 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HCT 116 human colorectal carcinoma cell line, generated through targeted disruption of the ACP1 gene. This polyclonal format ensures genetic heterogeneity while maintaining consistent loss of ACP1 protein expression, providing a robust model for studying the functional consequences of ACP1 ablation in a widely used cancer background.
HCT 116 is a well-characterized human colorectal carcinoma cell line of epithelial origin, harboring a KRAS G13D mutation and exhibiting microsatellite stability (MSS) with a near-diploid karyotype. It serves as a standard model for colorectal cancer research, particularly for investigating oncogenic KRAS-driven signaling, drug resistance, and tumor progression.
ACP1 encodes a low molecular weight phosphotyrosine phosphatase that dephosphorylates growth factor receptors such as EGFR, PDGFR, and VEGFR, along with signaling adaptors including p190RhoGAP, thereby attenuating tyrosine kinase signaling. Its activity is modulated by upstream regulators including EGF, PDGF, insulin, and Src kinases, and in turn it directly influences downstream pathways such as MAPK/ERK and PI3K/AKT. Additionally, ACP1 regulates cytoskeletal dynamics through RhoA/ROCK signaling, interacting with ??-catenin and Ephrin receptors to coordinate cell migration and adhesion.
In the HCT 116 colorectal cancer context, loss of ACP1 is anticipated to alter the balance of phospho-signaling networks, particularly given the co-occurring KRAS mutation. ACP1 deficiency may potentiate MAPK/ERK and PI3K/AKT pathway activation, mimicking aspects of oncogenic addiction and offering a platform to evaluate compensatory signaling mechanisms. Furthermore, deregulation of RhoA activity through ACP1 loss can modify cell motility and invasiveness, making this polyclonal knockout model highly relevant for studying colorectal cancer metastasis and the cytoskeletal contributions to tumor progression.
This polyclonal knockout cell model is suitable for a broad spectrum of experimental applications, including phospho-signaling analysis via Western blotting for phosphorylated tyrosine and phospho-RTK arrays, RhoA activity assays, and cell migration/invasion studies. It enables dissection of ACP1-dependent regulation of EGFR/PDGFR-Src-RhoA/ROCK-MAPK/ERK signaling cascades and investigation of drug resistance mechanisms in colorectal cancer. Co-immunoprecipitation assays can probe altered protein interactions with ACP1 substrates. Researchers may contact Ascent Research for additional technical details and experimental guidance.
