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Contributor Information

  • Name Ji?Ă­ NeuĹžil
  • Institute Institute of Biotechnology of the Academy of Sciences of the Czech Republic
  • Primary citation Ezrova et al. Oncogene. 2021 Apr, 40(14):2539-2552. PMID: 33686239

Tool Details

  • Tool name: PANC-1 SMAD4 KO cell line
  • Alternate names: PANC-1 SMAD4-deficient cells
  • Tool type: Cell line
  • Parental cell line: PANC-1
  • Organism: Human
  • Tissue: Pancreas
  • Gender: Male
  • Cancer type: Pancreatic ductal adenocarcinoma
  • Disease: Cancer
  • Morphology: Epithelial cells
  • Growth properties: Adherent
  • Model: Knock out
  • CRISPR: Yes
  • Conditional: No
  • Products or characteristics of interest: Crispr/Cas9 gene knock out
  • Description: SMAD4 is an important tumor suppressor involved in transforming growth factor ? (TGF?) signaling, and associated with altered mitochondrial activity. The resistance of SMAD4-deficient cells is mediated by increased mitophagic flux driven by MAPK/ERK signaling, whereas TGF?-induced resistance is autophagy-independent and linked to epithelial-to-mesenchymal transition (EMT). Mitochondria-targeted tamoxifen, a complex I inhibitor under clinical trial, overcomes resistance mediated by SMAD4-deficiency or TGF? signaling. Our data point to differential mechanisms underlying the resistance to treatment in PDAC arising from TGF? signaling and SMAD4 loss, respectively.
  • Research area: Pancreatic ductal adenocarcinoma

  • For Research Use Only

Target Details

Application Details


  • Growth medium: DMEM+10% FBS
  • Temperature: 37C
  • Atmosphere: 5% CO2
  • Storage medium: Complete medium + 10% DMSO
  • Storage conditions: Liquid Nitrogen
  • Shipping conditions: Dry Ice
  • Subculture routine: Trypsin-EDTA
  • Cultured in antibiotics?: Yes
  • Mycoplasma free: Yes
  • Biosafety level: 1


  • Available on request


  •   Ezrova et al. Oncogene. 2021 Apr, 40(14):2539-2552. PMID: 33686241