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Lysosomal Degradation Pathways Target Mutant Calreticulin and the Thrombopoietin Receptor in Myeloproliferative Neoplasms

Kaur, A.; Venkatesan, A.; Kandarpa, M.; Talpaz, M.; Raghavan, M.

2023-07-12 cancer biology
10.1101/2023.07.12.548605 bioRxiv
Show abstract

Somatic mutants of calreticulin (CRT) drive myeloproliferative neoplasms (MPNs) via binding to the thrombopoietin receptor (MPL) and aberrant activation of the JAK/STAT pathway. Compared with healthy donors, platelets from MPN patients with CRT mutations display low cell surface MPL. Co-expression of MPL with an MPN-linked CRT mutant (CRTDel52) reduces cell surface MPL expression, indicating the involvement of induced protein degradation, a better understanding of which could lead to new therapies. We show that lysosomal degradation is relevant to the turnover of both CRTDel52 and MPL. Drug-mediated activation of lysosomal degradation reduces CRTDel52 and MPL expression, with parallel inhibition of CRTDel52-induced cell proliferation and stem cell colony formation. Thus, reduced surface MPL, a marker of platelets from MPN patients with CRT mutations, results from mutant CRT-induced lysosomal degradation of MPL. Drug-induced activation of lysosomal degradation compromises the pathogenic effects of CRTDel52, which can be further exploited for therapeutic interventions.

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