Table 1.

Regulation of DNA repair genes after inhibition of the EGFR-src pathway

HCT116HT29HCT116HT29
src+src−src+src−src+src−src+src−
NERRecombination
ERCC12.150.891.821.12Holiday junction resolution
XPF0.871.041.121.23Rad512.231.872.983.12
XPG/ERCC52.893.454.143.85XRCC21.841.871.681.79
XPC1.541.651.791.67XRCC33.454.234.234.75
XPA1.972.030.841.02BLM2.212.032.452.2
WRN3.213.122.893.45
NHEJBRCA23.213.122.893.45
XRCC40.520.460.770.64TOP31.441.563.123.06
exo11.021.230.940.92Mus810.981.150.840.94
Eme14.521.74.891.62
DNA damage
Sensor/transducerTOPO I processing complex
NBS10.940.920.851.23Fen12.11.311.340.48
Rad501.261.120.780.84TOPO I1.120.951.231.17
MRE111.511.311.131.23PNPK1.230.950.840.78
rpa22.92.43.84.1XRCC10.840.741.540.91
BRCA12.12.32.822.9TDP11.421.121.480.98
Rad170.80.841.771.99
  • NOTE: HCT116- or HT29-growing cells were treated with SN38 for 24 h (HCT116, 2.5 nmol/L; HT29, 3.7 nmol/L), in the presence or absence of cetuximab (2.5 μg/mL) and SKI606 (10 μmol/L; indicated src+ or src− for simplicity on the table). Cells were then washed and further treated for 12 h by cetuximab-SKI606. The expression of the indicated mRNAs was then evaluated by quantitative RT-PCR experiments (n = 5).