Pro-survival role of protein kinase C epsilon in Philadelphia chromosome positive acute leukemia.

Abstract:

:Durable responses to imatinib monotherapy are rarely seen in aggressive forms of Philadelphia chromosome positive (Ph+) leukemias. To investigate the possible cause of treatment failure we examined the role of protein kinase C epsilon (PKCE), an oncogene highly implicated in the development of solid tumors and resistance to chemotherapy. We found high levels of PKCE transcripts in Ph+ acute lymphoblastic leukemia (ALL) cells from patients and cell lines, and imatinib resistant chronic myeloid leukemia, which were also less responsive to imatinib-induced apoptosis than Ph+ cells with lower PKCE expression. Furthermore, the siRNA-mediated knockdown or peptide inhibition of PKCE in Ph+ cells increased imatinib-induced apoptosis while overexpression of PKCE reduced imatinib-induced apoptosis, with concomitant increase in the pro-survival factor AKT. Our results suggest PKCE plays a protective role against apoptosis induced by BCR-ABL inhibition in Ph+ leukemias with high PKCE expression, such as Ph+ ALL.

journal_name

Leuk Lymphoma

journal_title

Leukemia & lymphoma

authors

Loi TH,Dai P,Carlin S,Melo JV,Ma DDF

doi

10.3109/10428194.2015.1043545

subject

Has Abstract

pub_date

2016-02-01 00:00:00

pages

411-418

issue

2

eissn

1042-8194

issn

1029-2403

journal_volume

57

pub_type

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