Back

Dual MAPK and HDAC inhibition rewires the apoptotic rheostat to trigger colorectal cancer cell death

Jenkins, L. J.; Luk, I. Y.; Palmieri, M.; Fairlie, W. D.; Lee, E. F.; Schoffer, K. L.; Tan, T.; Ng, I.; Vukelic, N.; Tse, J. W.; Nightingale, R.; Alam, Z.; Iatropoulos, G.; Ernst, M.; Afshar-Sterle, S.; Desai, J.; Gibbs, P.; Sieber, O.; Dhillon, A.; Tebbutt, N. C.; Mariadason, J. M.

2021-02-16 cancer biology
10.1101/2021.02.15.431252 bioRxiv
Show abstract

The EGFR/RAS/MEK/ERK signalling pathway (ERK/MAPK) is hyper-activated in most colorectal cancers (CRCs). A current limitation of inhibitors of this pathway is that they primarily induce cytostatic effects in CRC cells. Nevertheless, these drugs do induce expression of pro-apoptotic factors, suggesting they may prime CRC cells to undergo apoptosis. As histone deacetylase inhibitors (HDACi) induce expression of multiple pro-apoptotic proteins, we examined whether they could synergize with ERK/MAPK inhibitors to trigger CRC cell apoptosis. Combined MEK/ERK and HDAC inhibition synergistically induced apoptosis in CRC cell lines and patient-derived tumour organoids in vitro, and attenuated Apc-initiated adenoma formation in vivo. Mechanistically this effect was mediated through induction of the BH3-only pro-apoptotic proteins BIM and BMF. Importantly, we demonstrate that this treatment paradigm can be tailored to specific MAPK genotypes in CRCs, by combining HDACi with EGFR, KRASG12C or BRAFV600 inhibitors in KRAS/BRAFWT; KRASG12C, BRAFV600E CRC cell lines respectively. These findings identify a novel ERK/MAPK genotype-targeted treatment paradigm for colorectal cancer.

Matching journals

The top 7 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.