Combined Casein Kinase II inhibition and epigenetic modulation in acute B-lymphoblastic leukemia.

ABSTRACT:

Background

The tumor suppressor protein phosphatase and tensin homolog (PTEN) is a key regulator of the PI3K/AKT pathway which is frequently altered in a variety of tumors including a subset of acute B-lymphoblastic leukemias (B-ALL). While PTEN mutations and deletions are rare in B-ALL, promoter hypermethylation and posttranslational modifications are the main pathways of PTEN inactivation. Casein Kinase II (CK2) is often upregulated in B-ALL and phosphorylates both PTEN and DNA methyltransferase 3A, resulting in increased PI3K/AKT signaling and offering a potential mechanism for further regulation of tumor-related pathways.

Methods

Here, we evaluated the effects of CK2 inhibitor CX-4945 alone and in combination with hypomethylating agent decitabine on B-ALL proliferation a

SUBMITTER: Richter A 

PROVIDER: S-EPMC6404304 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature