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. 2021 Dec 13;10:e69729. doi: 10.7554/eLife.69729

Figure 7. Expression of RPL24, EEF2K, and EEF2 is consistent with increased eEF2 activity in colorectal cancer (CRC) tumours.

(A) Schematic of the findings presented here from pre-clinical mouse models. KRAS activation requires RPL24 expression to maintain low eEF2 phosphorylation. This occurs via a double negative regulation of eEF2K, whereby RPL24 suppresses eEF2K, which suppresses eEF2. eEF2 activity correlates with protein synthesis and proliferation rates. Dashed lines indicate indirect or undefined regulatory pathways. (B) RNA expression levels of RPL24, EEF2K, and EEF2 between normal colon and colon adenocarcinoma samples using data extracted from The Cancer Genome Atlas by TNMplot. Relative expression changes are annotated, as well as p values for each transcript.

Figure 7.

Figure 7—figure supplement 1. Expression of RPL24, EEF2K, and EEF2 suggest increased eEF2 activity in colorectal cancer (CRC) tumours.

Figure 7—figure supplement 1.

(A) Protein levels of RPL24, eEF2K, and eEF2 in normal colon and colon adenocarcinoma collated from the Clinical Proteomic Tumor Analysis Consortium by UALCAN. Numbers of samples and p values are shown for each protein. (B) RNA expression levels of RPL24, EEF2K, and EEF2 between normal rectum and rectum adenocarcinoma samples using data extracted from The Cancer Genome Atlas by TNMplot. Relative expression changes are annotated, as well as p values for each transcript.