Fig. 1: Single inhibition of mutant KRAS was not sufficient to abrogate cell viability in CRC-PDCs. | npj Precision Oncology

Fig. 1: Single inhibition of mutant KRAS was not sufficient to abrogate cell viability in CRC-PDCs.

From: Mechanisms of KRAS inhibitor resistance in KRAS-mutant colorectal cancer harboring Her2 amplification and aberrant KRAS localization

Fig. 1

a, b Evaluation of sensitivity to KRAS inhibitors. Cells were treated with 1 µM of sotorasib or 30 nM of MRTX1133 for 72 h. Cell viability was detected by CellTiter-Glo assay, and the relative cell viability to the non-treated condition was calculated. Data were expressed as mean ± SD. c Confirmation of the KRAS downstream signal in KRAS inhibitor treatment. KRAS-G12C and KRAS-G12D CRC cell lines were exposed to 1 µM of sotorasib or 100 nM of MRTX1133 treatment. The cell lysates were collected at each time point and immunoblotted to detect the indicated antibodies (left). d Evaluation of KRAS dependency in KRAS-mutated PDCs. The cell viability was measured by CellTiter-Glo assay, and the relative cell viability to si-ctrl cells was calculated. Data were expressed as mean ± SD.

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