In Stock Cell Lines
Homo sapiens (Human)
Large intestine (colon)
Adherent
The APC Knockout HCT 116 Cell Line is a CRISPR/Cas9-edited knockout model derived from human epithelial colorectal adenocarcinoma HCT 116 cells. By disrupting the tumor suppressor APC, it stabilizes ??-catenin (CTNNB1) and drives constitutive TCF/LEF-mediated transcription of oncogenes such as MYC and CCND1, mirroring APC loss in colorectal cancers. This knockout line is a powerful tool for studying Wnt/??-catenin signaling, colorectal cancer pathogenesis, and chromosomal instability. It supports drug screening of Wnt inhibitors and functional assays including TOP/FOP flash reporter, proliferation, and invasion studies, exploiting the HCT 116 background with KRAS G13D, PIK3CA H1047R, and CTNNB1 S45 mutations.
NALF2 Knockout HEK293T Cell Line
Cat. No. ARG43990
MFGE8 Knockout KYSE150 Polyclonal Cells
Cat. No. ARG12274
IGF1R Knockout AGS Polyclonal Cells
Cat. No. ARG27017
KCTD1 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG30093
KCTD1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31815
GLYR1 Knockout AGS Polyclonal Cells
Cat. No. ARG2616
The APC Knockout HCT 116 Cell Line is a CRISPR/Cas9-edited knockout cell line originating from the human HCT 116 colorectal adenocarcinoma line. It provides a stable loss-of-function model for the tumor suppressor APC, enabling detailed functional studies without confounding endogenous protein. This knockout line faithfully recapitulates APC inactivation events prevalent in colorectal cancers.
HCT 116 is a male-derived colorectal carcinoma cell line exhibiting microsatellite instability and established driver mutations: KRAS G13D, PIK3CA H1047R, and CTNNB1 S45 deletion. These features render it a clinically relevant model for KRAS/PI3K/Wnt-co-altered tumors. Its partial ??-catenin stabilization sensitizes the line to further pathway activation upon APC loss.
APC functions as an essential scaffold in the ??-catenin destruction complex, which also comprises AXIN1, GSK3B, and CK1??. In unstimulated cells, this complex phosphorylates ??-catenin, marking it for ubiquitination and proteasomal degradation. APC knockout dismantles the complex, leading to ??-catenin stabilization, nuclear accumulation, and TCF/LEF-dependent transcription of pro-proliferative genes including MYC, CCND1, and AXIN2. Upstream, APC activity is governed by WNT3A/WNT1 binding to Frizzled/LRP receptors, while downstream it interacts with proteins such as AMER1, DLG1, and PPP2CA, implicating additional roles in adhesion and microtubule organization.
In the HCT 116 context, APC knockout cooperates with the endogenous CTNNB1 mutation to yield maximal ??-catenin signaling, mimicking the frequent APC/CTNNB1 co-alterations in colorectal tumors. This synergy drives enhanced proliferation, invasion, and chromosomal instability phenotypes. The cell line’s epithelial character and tumorigenic potential in xenografts make it an ideal platform for investigating APC’s tumor-suppressive mechanisms in a disease-relevant background.
Applications span multiple domains of colorectal cancer research. It is extensively used for Wnt pathway dissection via western blotting for active ??-catenin, RT-qPCR of MYC/AXIN2, and TOP/FOP flash reporter assays. Drug discovery efforts employ it for high?throughput screening of Wnt inhibitors using MTT proliferation and Transwell invasion assays. Co?immunoprecipitation experiments elucidate destruction complex integrity, while colony formation assays assess long-term growth effects. In vivo, it supports tumor xenograft models for pharmacodynamic studies. For additional details, please reach out to Ascent Research.
