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Table 1 Overview of GAPDH expression in different tumor and non-tumor cell lines as a consequence of the development of a hypoxic cellular microenvironment.

From: Absence of GAPDH regulation in tumor-cells of different origin under hypoxic conditions in – vitro

Cell line or type Origin Genetic mutations GAPDH overexpression Ref. Ref.
   (-/+) under hypoxia GAPDH mutations
U373 – MG Malignant glioma cells (Human) -Apoptosis resistant mutant P53 (-) [24, 25] [40],
   -Peroxisome proliferator activated receptor – γ    
   -PTEN mutation    [41],
GaMG Malignant glioma cells (Human) (-) (-) [24, 25] [33], [41]
U251 malignant glioma cells (Human) Mutated p53 (-) [24, 25] [40]
   P14ARF/P16 deletion    
Bovine articular chondrocytes Chondrocytes (Bovine) Not determined (-) [37] (-)
LNCap Prostate adenocarcinoma cells (-) (+) [34] [27]
  (Human)     
ATII Alveolar epithelial cells (Rat) (-) (+) [26] [26]
SiHA Spontaneous cervical cancer cells (Human) (-) (+) [35] [36]
   Wild type p53    
MBEC4 Brain capillary endothelial cells (-) (+) [37] [37]
  (Mouse)     
EC Endothelial cells (Human) - Not determined (+) [5], [22], [23], [24, 39], [39] [39]
   - Mutated epithelial cells are present    
HepG2 Human Hepatocellular Carcinoma Raf inactive (-) (-) [This Paper] [42], [43]
   Wild type p53    
   Wild type Retinoblastoma    
Hep-3-B Human Hepatocellular Carcinoma Wild type p53 (-) [This Paper] [43, 44]
   Absence of RB transcripts    
   Deletion p53 gene    
Hep.1-6 Mouse Hepatocellular Carcinoma - Not determined (-) [This Paper] [45]
HCT-116 Colon cancer cell line (Human) K-ras (+) (-) (-) [46]
HT-29 Colon cancer cell line (Human) (-) (-) (-) [46], [47]
A-549 Lung cancer cell line (Human) k-Ras (+) (-) (-) [47], [48]
   c-RAS (+)