In Stock Cell Lines
Mus musculus (Mouse)
Breast (mammary gland)
Adherent
The XBP1 Knockout EO771 Cell Line is a CRISPR/Cas9-edited knockout cell line of the murine EO771 triple-negative breast cancer model, in which the gene encoding the UPR transcription factor XBP1 has been disrupted. This loss-of-function model enables investigation of ER stress signaling in an aggressive mammary adenocarcinoma background. XBP1, activated by IRE1-mediated mRNA splicing, transcriptionally regulates ER chaperones such as BiP/HSPA5 and components of ER-associated degradation. Applications include studying tumor cell adaptation, drug resistance, and UPR-dependent survival mechanisms using assays such as Western blotting and viability testing under ER stress.
NFKBIA Knockout CAL-27 Cell Line
Cat. No. ARG43997
ARHGAP1 Knockout A2780 Polyclonal Cells
Cat. No. ARG28764
INSR Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30835
ARL6IP1 Knockout A549 Polyclonal Cells
Cat. No. ARG31698
MAPK7 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6053
PCYOX1L Knockout 786-O Polyclonal Cells
Cat. No. ARG5110
The XBP1 Knockout EO771 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the EO771 murine mammary adenocarcinoma cell line, engineered to disrupt the XBP1 gene. This knockout model enables loss-of-function studies of XBP1, a critical transcription factor in the unfolded protein response (UPR). The cell line serves as a stable tool for investigating ER stress signaling pathways.
EO771 is a well-characterized triple-negative breast cancer (TNBC) cell line originating from a spontaneous mammary adenocarcinoma in a C57BL/6 mouse. These cells represent an aggressive, basal-like breast cancer subtype that lacks estrogen receptor, progesterone receptor, and HER2 amplification, making them a valuable syngeneic model for studying tumorigenesis, metastasis, and therapeutic resistance in immunocompetent hosts.
XBP1 is a key transducer of the UPR, activated downstream of the ER stress sensor IRE1 (ERN1). Upon ER stress, IRE1 catalyzes unconventional splicing of XBP1 mRNA, yielding the active transcription factor XBP1s. XBP1s translocates to the nucleus and transcriptionally regulates expression of ER chaperones (e.g., BiP/GRP78/HSPA5), protein disulfide isomerases (e.g., PDIA4), ER-associated degradation components (e.g., EDEM1, OS9), and genes involved in lipid synthesis. XBP1 interacts with cofactors such as NF-Y, CREB, and p300/CBP, and its activity is modulated by ATF6 and PERK branches of the UPR. Downstream, XBP1 also controls the expression of pro-inflammatory cytokine IL-6 and components facilitating ER homeostasis.
In the context of TNBC, XBP1 contributes to tumor cell adaptation to the hostile tumor microenvironment, where hypoxia, nutrient deprivation, and oxidative stress activate the UPR. Disruption of XBP1 in EO771 cells provides a powerful system to dissect its role in promoting cancer cell survival, invasion, and resistance to chemotherapeutics. This model is particularly relevant for exploring the dependency of aggressive breast cancers on ER stress response pathways and for identifying synthetic lethal interactions.
Researchers can employ this knockout line to perform detailed functional studies, including Western blotting and RT-qPCR to quantify XBP1 splicing and expression of ER stress markers, RNA-seq to profile transcriptional changes, and immunofluorescence to visualize ER stress responses. Cell-based assays such as viability assays under treatment with ER stress inducers (e.g., tunicamycin, thapsigargin), migration and invasion assays, and drug sensitivity testing can delineate the role of XBP1 in therapeutic response. This knockout cell line is a versatile resource for functional genomics screens and target gene identification in breast cancer research. For further technical details, please contact Ascent Research.
