The ATF2 Knockout HT29 Polyclonal Cells constitute a genetically engineered polyclonal population of the human colorectal adenocarcinoma cell line HT29, modified through CRISPR/Cas9-mediated disruption of the ATF2 (Activating Transcription Factor 2) gene. This loss-of-function model allows for systematic investigation of ATF2-dependent transcriptional programs in a well-characterized intestinal epithelial background. The polyclonal knockout format reflects a heterogeneous pool of edited cells, enabling robust functional studies without clonal selection artifacts.
HT29 cells were originally derived from a primary colorectal adenocarcinoma resected from a 44-year-old female patient. This adherent epithelial cell line is widely utilized in cancer biology research, particularly for studies of colorectal tumorigenesis, intestinal differentiation, and response to therapeutic agents. HT29 cells exhibit a moderate degree of differentiation and retain functional signaling cascades relevant to colorectal cancer, including the MAPK and TGF-?? pathways, making them an appropriate host for interrogating stress-responsive transcription factors like ATF2.
ATF2 is a basic leucine zipper (bZIP) transcription factor that integrates stress signals primarily through the JNK and p38 MAPK pathways. It is activated by upstream kinases including JNK, p38 MAPK, MKK3/6, MEKK1, ATM, and ATR, and mediates cellular responses to stimuli such as TNF-?? and ultraviolet radiation. ATF2 forms heterodimers with c-Jun and homodimers with itself, and interacts with co-regulators like p300, HDAC1, Smad3, BRCA1, and JDP2. It possesses intrinsic histone acetyltransferase activity and transcriptionally regulates a network of downstream targets including cyclin D1 (CCND1), c-Jun (JUN), Bcl-2, p53 (TP53), MMP2, and IFNB1, thereby controlling cell cycle progression, apoptosis, DNA damage repair, and extracellular matrix remodeling.
Disruption of ATF2 in HT29 colorectal cancer cells impairs transcriptional control of stress-responsive genes critical for cell survival and proliferation. Specifically, loss of ATF2 attenuates JNK/p38-driven pro-survival signaling, potentially sensitizing the cells to genotoxic stress and reducing tumorigenic capacity. This knockout model provides a valuable tool to dissect ATF2??s role in mediating the balance between apoptosis and cell cycle progression in a colorectal adenocarcinoma background, and to evaluate how loss of ATF2 affects downstream effectors such as cyclin D1, c-Jun, and p53 under various stress conditions.
This cell model is suited for a wide array of experimental applications, including functional investigation of ATF2 in colorectal cancer biology, stress response pathway analysis, drug sensitivity and resistance profiling, transcriptional regulation studies, and tumorigenesis or metastasis assays. Representative assays include western blotting for ATF2 and phospho-JNK/p38, RT-qPCR for target genes like CCND1 and Bcl-2, flow cytometry for apoptosis and cell cycle analysis, colony formation and MTT proliferation assays, migration/invasion assays, and ChIP-qPCR to map ATF2 occupancy on promoters. For additional information or to place an order, please contact Ascent Research.
