Back

Inhibition of proprotein convertase subtilisin-like kexin type 9 (PCSK9) potentiates anti-angiogenic therapy in colorectal cancer liver metastases

Rada, M.; Reynolds, A. R.; Lazaris, A.; Seidah, N.; Metrakos, P.

2023-05-29 molecular biology
10.1101/2023.05.29.542731 bioRxiv
Show abstract

Colorectal cancer liver metastatic (CRCLM) tumours present as two main histopathological growth patterns (HGPs) including desmoplastic HGP (DHGP) and replacement HGP (RHGP). The DHGP tumours obtain their blood supply by sprouting angiogenesis, whereas the RHGP tumours utilize an alternative vascularisation known as vessel co-option. In vessel co-option, the cancer cells hijack the mature sinusoidal vessels to obtain blood supply. Vessel co-option has been reported as an acquired mechanism of resistance to anti-angiogenic treatment in CRCLM. Herein, we showed that inhibiting proprotein convertase subtilisin-like kexin type 9 (PCSK9) via clinically approved PCSK9-neutralizing antibody (Evolocumab) can boost the response of vessel co-opting tumours to anti-angiogenic therapy. Mechanistically, we found that PCSK9 inhibition downregulates runt related transcription factor-1 (RUNX1) expression levels in CRCLM cancer cells in vivo, which its expression positively correlates with the development of vessel co-option. Collectively, these results suggest that inhibiting PCSK9 is a promising way to improve the efficacy of anti-angiogenic therapy against vessel co-opting tumours in CRCLM.

Matching journals

The top 8 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.