PIM Kinase Pathways in Oncogenesis and Therapeutics
Summary
PIM kinases are a family of constitutively active serine/threonine protein kinases comprising three isoforms (PIM1, PIM2 and PIM3). They integrate extracellular cues via JAK/STAT and receptor tyrosine kinase pathways to regulate diverse cellular processes, including cell cycle progression, inhibition of apoptosis, metabolic adaptation and cytoskeletal remodelling. Aberrant PIM expression is observed across haematological and solid malignancies, where it drives proliferation, survival, resistance to chemotherapy and invasive behaviour. Therapeutic strategies have evolved from ATP-competitive inhibitors to emerging approaches such as proteolysis targeting chimeras (PROTACs) and combination regimens with PI3K/AKT/mTOR, MAPK or DNA-damage response inhibitors. Preclinical models reveal that selective degradation or co-targeted inhibition of PIM kinases can overcome compensatory signalling networks and attenuate tumour growth and metastasis, highlighting both challenges and opportunities in the clinical translation of PIM-directed therapies.
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PIM Kinase Pathways in Oncogenesis and Therapeutics publication trend
The graph below shows the total number of articles in pim kinase pathways in oncogenesis and therapeutics across all publications each year (not limited to Nature Index journals).
Technical terms
PIM kinases: A family of constitutively active serine/threonine kinases (PIM1, PIM2, PIM3) involved in cell survival, proliferation and oncogenesis.
Proteolysis targeting chimera (PROTAC): A bifunctional molecule that recruits an E3 ubiquitin ligase to induce selective degradation of a target protein via the ubiquitin–proteasome system.
Wave regulatory complex (WRC): A multiprotein assembly that activates the Arp2/3 complex to drive actin polymerisation, membrane protrusion and cell motility.
ATP-competitive inhibitor: A small molecule that occupies the ATP-binding pocket of a kinase, blocking its catalytic activity.
References
- Targeting Pim kinases in hematological cancers: molecular and clinical review. Molecular Cancer (2023).
- PIM1 targeted degradation prevents the emergence of chemoresistance in prostate cancer. Cell Chemical Biology (2023).
- PIM1 phosphorylates ABI2 to enhance actin dynamics and promote tumor invasion. Journal of Cell Biology (2023).
- PIM kinase inhibition: co-targeted therapeutic approaches in prostate cancer. Signal Transduction and Targeted Therapy (2020).
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