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Protein kinase C alpha-mediated phosphorylation of PIM-1L promotes the survival and proliferation of acute myeloid leukemia cells.

Author: KatayamaKazuhiro, NoguchiKohji, SugimotoYoshikazu, TakamiMayu

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.

Overview

FLT3-ITD, a constitutively active mutant of FLT3, is found in 20-30% of acute myeloid leukemia (AML) cases. This study investigated the role of protein kinase C (PKC)-mediated phosphorylation on the expression and function of PIM-1L, a pro-survival protein upregulated by FLT3-ITD. It was found that PKCα directly phosphorylates PIM-1L, stabilizing the protein and enhancing its kinase activity, promoting AML cell survival and proliferation.
Paper Details　
Original Abstract of the Article :
FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) is a constitutively active mutant of FLT3 and causes 20%-30% of acute myeloid leukemia (AML) cases. FLT3-ITD upregulates the proviral integration site for Moloney murine leukemia virus 1 (PIM-1) expression and promotes the prolifera...See full text at original site
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引用元：
https://doi.org/10.1016/j.bbrc.2018.07.049

データ提供：米国国立医学図書館（NLM）

PIM-1L: A Crucial Player in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) is a complex and aggressive cancer of the blood. This study delves into the role of PIM-1L, a protein involved in cell survival and proliferation, in the development of AML. The researchers investigated the influence of protein kinase C (PKC) on PIM-1L activity, unraveling a crucial mechanism that contributes to the progression of AML. It's like studying the intricate network of pathways that govern the growth and survival of a desert ecosystem, seeking to understand the critical role of PIM-1L in AML.

PKC's Impact on PIM-1L Activity

The study found that PKCα directly phosphorylates PIM-1L, leading to increased stability and kinase activity. This phosphorylation event promotes the survival and proliferation of AML cells. The researchers discovered that inhibiting PKCα with the drug sotrastaurin significantly suppressed the growth of AML cells. It's like finding a crucial lever in a complex machine, where inhibiting PKCα activity can disrupt the growth and spread of AML.

Dr.Camel's Conclusion

This study provides valuable insights into the role of PIM-1L and PKCα in AML development. The findings suggest that targeting PKCα could be a promising strategy for developing new therapies to combat this aggressive form of leukemia. It's like a camel adapting to a changing environment, harnessing new knowledge and tools to overcome a formidable obstacle. This research offers hope for the future of AML treatment, bringing us closer to a world where this devastating disease is effectively managed.

Date :
  1. Date Completed 2019-02-18
  2. Date Revised 2019-02-19
Further Info :

Pubmed ID

30017192

DOI: Digital Object Identifier

10.1016/j.bbrc.2018.07.049

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