An article published this year in “ONCOTARGET” using our FITC
Annexin V Apoptosis Detection Kit with PI, by our customers from Department
of Medicine, Hematology and Clinical Immunology Section, University of Padova,
Padova, Italy, in the analysis of how Inactivation of CK1α in multiple myeloma
empowers drug cytotoxicity by affecting AKT and β-catenin survival signaling
pathways. Congrats and Thanks.
Summary:
Recent evidence indicates that
protein kinase CK1α may support the growth of multiple myeloma (MM) plasma
cells. Here, by analyzing a large cohort of MM cases, we found that high CK1α
mRNA levels are virtually associated with all MM patients. Moreover, we
provided functional evidence that CK1α activity is essential for malignant
plasma cell survival even in the protective niche generated by co-cultures with
bone marrow stromal cells. We demonstrated that CK1α inactivation, while toxic
for myeloma cells, is dispensable for the survival of healthy B lymphocytes and
stromal cells. Disruption of CK1α function in myeloma cells resulted in
decreased Mdm2, increased p53 and p21 and reduced expression of β-catenin and
AKT. These effects were mediated partially by p53 and caspase activity.
Finally, we discovered that CK1α inactivation enhanced the cytotoxic effect of
both bortezomib and lenalidomide. Overall, our study supports a role for CK1α
as a potential therapeutic target in MM in combination with proteasome
inhibitors and/or immunomodulatory drugs.
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