BxPC-3

BxPC-3

Cat.No.: CSC-C9163W

Species: Homo sapiens (Human)

Source: Pancreas

Morphology: epithelial

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Cat.No.
CSC-C9163W
Description
The cells do not express the cystic fibrosis transmembrane conductance regulator (CFTR).
Species
Homo sapiens (Human)
Source
Pancreas
Recommended Medium
90% RPMI1640 + 10% h.i. FBS
Morphology
epithelial
Disease
Pancreatic Ductal Adenocarcinoma
Storage and Shipping
liquid nitrogen vapor phase
Synonyms
BxPc-3; BXPC-3; Bx-PC3; BXPC3; BxPC3; BxPc3; Biopsy xenograft of Pancreatic Carcinoma line-3
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

BxPC-3 is a well-characterized human pancreatic ductal adenocarcinoma (PDAC) cell line established from a primary pancreatic tumor of a 61-year-old female. It exhibits epithelial morphology, adherent growth, and robust expansion in standard culture. It is tumorigenic in immunodeficient mice and supports subcutaneous and orthotopic xenograft models, enabling in vitro and in vivo studies of pancreatic cancer biology.

A key advantage is that BxPC-3 is KRAS wild-type, distinguishing it from most PDAC lines and patient tumors, which frequently harbor KRAS mutations. This makes BxPC-3 a valuable model for the clinically distinct KRAS wild-type subset of pancreatic cancer and a useful comparator for KRAS-mutant lines such as Panc-1 and Mia PaCa-2. It is widely used to study tumor progression, chemoresistance, radiation response, cancer stem cell biology, and biomarker discovery, as well as for drug screening and target validation. Its well-characterized genomic and transcriptomic profiles, commercial availability, and reproducible growth support comparative and high-throughput studies. BxPC-3 is amenable to transfection, siRNA/CRISPR perturbation, flow cytometry, immunostaining, Western blot, qPCR, co-culture, and 3D models.

Role of Octamer Transcription Factor 4 in Proliferation, Migration, Drug Sensitivity, and Stemness Maintenance of Pancreatic Cancer Cells

To investigate the role of octamer transcription factor 4 (OCT4) in pancreatic cancer stem cells (CSCs) and its effect on pancreatic cancer (PC) cell proliferation, migration, drug sensitivity, and stemness maintenance.

BxPC-3 cells were used to assess the effects of OCT4 modulation on cellular behavior. Proliferation, migration, and stemness of BxPC-3 cells were evaluated, and the PI3K/AKT/mTOR pathway was examined to gain mechanistic insights.

OCT4 modulation altered BxPC-3 cell proliferation, invasion, and stemness, with OCT4 overexpression (OV-OCT4) enhancing these properties and OCT4 interference decreasing them. OV-OCT4 activated the PI3K/AKT/mTOR pathway, which correlated with an increase in PC stem cells (PCSC).

Change in the role of OCT4 expression upon proliferation of BxPC3 cells.
Fig. 1. Change in the proliferation of BxPC3 cells upon high and low expression of Octamer transcription factor 4 (Shi, Xue-Ying, et al., 2025).
BxPC3 tumor sphere formation and the expression change of OCT4 related to the stemness of BxPC3 cells.
Fig. 2. Tumor sphere formation and change in the stemness of BxPC3 cells with high and low expression of Octamer transcription factor 4 (Shi, Xue-Ying, et al., 2025).

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