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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 (+)