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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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PIM3 Kinase: A Promising Novel Target in Solid Cancers.

Pinar Atalay1, Bulent Ozpolat1,2

  • 1Department of Nanomedicine, Houston Methodist Research Institute, Houston, TX 77030, USA.

Cancers
|February 10, 2024
PubMed
Summary

Provirus-integrating Moloney site 3 (PIM3) kinase is a proto-oncogene overexpressed in many cancers. Inhibiting PIM3 shows promise for suppressing tumor growth and metastasis, highlighting its potential as a cancer therapeutic target.

Keywords:
PIM kinase inhibitorsPIM3serine/threonine kinasesolid cancertargeted therapiestriple-negative breast cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Provirus-integrating Moloney site 3 (PIM3) is a serine/threonine kinase and proto-oncogene.
  • PIM3 is frequently overexpressed in cancers from endoderm-derived tissues, including liver, pancreas, colon, stomach, prostate, and breast.
  • Overexpressed PIM3 drives cancer cell proliferation, survival, invasion, tumor growth, metastasis, and therapy resistance.

Purpose of the Study:

  • To review recent developments on the role of PIM3 in various cancers.
  • To explore the potential of PIM3 as a novel molecular target for cancer therapy.
  • To discuss the current status of PIM-targeted therapies in clinical trials.

Main Methods:

  • Literature review of recent studies on PIM3 function and targeted therapies.
  • Analysis of PIM3's role in oncogenic signaling pathways.
  • Examination of preclinical data on genetic inhibition of PIM3.

Main Results:

  • Genetic inhibition of PIM3 suppressed in vitro proliferation and in vivo tumor growth and metastasis in preclinical models.
  • PIM3 activation promotes cancer progression and resistance to chemotherapy and radiation.
  • PIM3 contributes to an immunosuppressive tumor microenvironment.

Conclusions:

  • PIM3 is a critical oncogene with significant potential as a therapeutic target in solid tumors.
  • While pan-PIM inhibitors are in early clinical trials for hematological cancers, no FDA-approved inhibitors currently exist for PIM3-targeted therapy.
  • Further research and clinical development are warranted to leverage PIM3 inhibition for cancer treatment.