In Stock Cell Lines
Homo sapiens (Human)
Pancreas
Adherent
The ITGB1 Knockout PANC-1 Cell Line is a CRISPR/Cas9-edited human pancreatic cancer cell model for studying integrin ??1 (ITGB1) function. ITGB1 encodes a cell adhesion receptor that mediates interactions with extracellular matrix proteins, activating downstream pathways involving FAK, Src, PI3K/AKT, and ERK, and regulating processes such as proliferation, survival, and migration. Derived from a KRAS-mutant pancreatic ductal adenocarcinoma, the PANC-1 background is ideal for investigating integrin-driven metastasis and drug resistance. Applications include cell adhesion and invasion assays, 3D tumor model studies, and phospho-signaling analysis to dissect integrin contributions to oncogenic signaling.
LIPA Knockout K562 Polyclonal Cells
Cat. No. ARG19467
EXPH5 Knockout A549 Polyclonal Cells
Cat. No. ARG10833
MFSD1 Knockout Hela Polyclonal Cells
Cat. No. ARG8837
BLOC1S3 Knockout huh-7 Polyclonal Cells
Cat. No. ARG28100
C5orf24 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG41513
MICU2 Knockout AGS Polyclonal Cells
Cat. No. ARG2370
The ITGB1 Knockout PANC-1 Cell Line is a CRISPR/Cas9-edited human pancreatic cancer cell line designed for loss-of-function investigation of integrin beta 1 (ITGB1). Generated by targeted disruption of the ITGB1 gene in PANC-1 cells, this constitutive knockout model abrogates ITGB1 protein expression and downstream integrin ??1-mediated functions. It provides a robust system to study adhesion signaling, tumor progression, and drug response mechanisms in a pancreatic ductal adenocarcinoma context.
PANC-1 is a KRAS, TP53, and CDKN2A-mutant pancreatic carcinoma cell line derived from a 56-year-old male. It serves as a clinically relevant model of pancreatic cancer possessing high invasive and metastatic potential. The cell line??s dependency on integrin-mediated adhesion makes it a valid platform to interrogate ITGB1-dependent phenotypes, given its expression of the ??1 integrin subunit and capacity for ECM interactions critical for tumor cell dissemination.
ITGB1 heterodimerizes with multiple ?? integrins (e.g., ITGA1-6, ITGAV) to bind ECM ligands including fibronectin, collagens, and laminins. Ligand engagement recruits talin and kindlin, which activate FAK and Src, triggering the PI3K/AKT and MAPK/ERK cascades. Downstream, Rho GTPases (RhoA, Rac1) reorganize the actin cytoskeleton, while transcription factors AP-1 and NF-??B drive expression of MMPs, cyclin D1, Bcl-2, and Snail. ITGB1 signaling integrates with growth factor cues via co-receptors such as EGFR and is modulated by tetraspanins CD9 and CD81.
In PANC-1 cells, ITGB1 knockout disrupts adhesion to fibronectin and collagen, attenuating FAK and ERK phosphorylation and reducing survival and proliferative outputs. Impaired migration and invasion are anticipated, given the integrin??s role in actin-based motility. In a KRAS-driven tumor model, the absence of ITGB1 signaling may uncouple matrix-dependent survival cues, offering a tool to examine integrin dependence in oncogenic signaling and potential synergies with gemcitabine therapy.
This knockout line is applicable in adhesion, spreading, and migration assays on defined ECM substrates, Boyden chamber invasion assays, and 3D spheroid cultures. Downstream analyses include Western blot detection of phospho-FAK/ERK, immunofluorescence labeling of focal adhesion proteins, RNA-seq transcriptomics, and drug sensitivity testing. Proliferation and apoptosis assays further define the integrin contribution to cell growth. For additional technical specifications or ordering inquiries, please contact Ascent Research.
