We propose that highly proliferative AML activate CHK1, affording protection against proliferation-associated RS. CHK1 upregulation occurs preferentially in immature and monocytic lineage committed AML, suggesting these subgroups may be optimal candidates for therapeutic intervention with CHK1 inhibitors.
Finally, in clinical samples, ovarian cancer patients with high levels of EZH2 and CHK1 not only were more resistant to platinum but also had a poorer prognosis. Our data revealed a previously unidentified functional and mechanistic link between EZH2 levels, CHK1 signaling activation, and ovarian CSCs and provided strong evidence that EZH2 promotes ovarian cancer chemoresistance and recurrence.
Additionally, CHEK1 expression might display intratumour heterogeneity, suggesting CHEK1 might be overexpressed in KRAS altered lung cancer cell clusters, which might provide a potential clue for future use of CHEK1 inhibitor targeted therapy for KRAS altered lung adenocarcinoma. Conclusion This study indicated CHEK1 is one of the key genes and could be used as a potential prognostic biomarker and therapeutic target for LUAD.
Finally, we demonstrated in vivo in xenograft models that CHEK1 overexpression prompted MM proliferation and drug resistance, while CHEK1 knockdown conversely inhibited MM growth. Together, these findings suggest that targeting the enzymatic catalytic center encoded by CHEK1 mRNA and circCHEK1_246aa is a promising therapeutic modality to target both MM cells and the BM niche.
8 months ago
CHEK1 (Checkpoint kinase 1)
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