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. 2015 Aug 1;6(29):28312–28326. doi: 10.18632/oncotarget.4873

Table 3. Correlation between RK-33 sensitivity and mutation status in colorectal cancer cell lines.

Cell line RK-33 Sensitivity Mutations MSI status
IC50 (μM) 95% CI APC Truncation TP53 RAS/RAF Others
HCT116* 2.71 2.64–2.80 KRAS PIK3CA, CTNNB1 MSI
CRC29 2.89 2.66–3.14 KRAS, BRAF SMAD4, STK11 MSI
HT29* 2.96 2.84–3.08 E853X, T1556fsX3 R273H BRAF PIK3CA, SMAD4 MSS
CR9 4.97 4.51–5.48 R1114X, S1503E R213X, V157A SMAD4, FBXW7, ERBB2
DLD-1* 5.36 5.15–5.59 I1417X S241F KRAS MSI
CRC47 5.54 5.07–6.05 R1450X P75LfsX48 PIK3CA MSI
SW480* 6.32 5.60–7.15 Q1338X R273H, P309S KRAS SMAD4 MSS
Colo205* 6.65 6.00–7.37 T1556fsX3 Y103fsX8 BRAF MSS
L145 8.77 7.63–10.08 S1436LfsX34 R110P KRAS MSS

The genomic background of colorectal cancer derived adherent cell lines and 3D cultures and their relative sensitivity to RK-33. Mutational status was derived from:

*

publicly available data in the CanSAR database.

next-generation sequencing.

no mutation detected.