ArticleOncogene2024
PIM1 drives lipid droplet accumulation to promote proliferation and survival in prostate cancer.
Article in Oncogene, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- PIM1-mediated signalling as a therapeutic target in breast cancer: repurposing venetoclax for targeted inhibition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Exploring PIM1 Kinase as a Therapeutic Target: Mechanisms and Strategies in Cancer Treatment.International journal of molecular sciences · 2026Review
- Aberrant activation of epigenetic BRD9-DGAT1 axis promotes lipid droplets deposition and ferroptosis resistance in YAP-high prostate cancer.Cell death & disease · 2026Article
- Lipolysis gone rogue: the HSL connection in feeding cancer.Cell biology and toxicology · 2025Review
- Polarization-Sensitive Holotomography for Multidimensional Label-Free Imaging and Characterization of Lipid Droplets in Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of Non-Coding Regions in Breast Cancer: From Gene Regulation to Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Novel Roles of the GPI-Anchor Cleaving Enzyme, GDE2, in Hippocampal Synaptic Morphology and Function.eNeuro · 2025Article
- Hypoxia induced lipid droplet accumulation promotes resistance to ferroptosis in prostate cancer.Oncotarget · 2025Article
- Kinome profiling reveals pathogenic variant specific protein signalling networks in MEN2 children with Medullary Thyroid Cancer.NPJ precision oncology · 2025Article
- Lipid Droplets Metabolism Mediated by ANXA7-PPARγ Signaling Axis Regulates Spinal Cord Injury Repair in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pim1 promotes the maintenance of bone homeostasis by regulating osteoclast function.Experimental & molecular medicine · 2025Article
- Adaptation mechanisms in cancer: Lipid metabolism under hypoxia and nutrient deprivation as a target for novel therapeutic strategies (Review).Molecular medicine reports · 2025Review
- Inflammation in cancer: therapeutic opportunities from new insights.Molecular cancer · 2025Review
- CPT1A-mediated MFF succinylation promotes stemness maintenance in ovarian cancer stem cells.Communications biology · 2025Article
- Combined Blockade of Lipid Uptake and Synthesis by CD36 Inhibitor and SCD1 siRNA Is Beneficial for the Treatment of Refractory Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State.Pigment cell & melanoma research · 2025Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Lipid droplets (LDs) are dynamic organelles with a neutral lipid core surrounded by a phospholipid monolayer. Solid tumors exhibit LD accumulation, and it is believed that LDs promote cell survival by providing an energy source during energy deprivation. However, the precise mechanisms controlling LD accumulation and utilization in prostate cancer are not well known. Here, we show peroxisome proliferator-activated receptor α (PPARα) acts downstream of PIM1 kinase to accelerate LD accumulation and promote cell proliferation in prostate cancer. Mechanistically, PIM1 inactivates glycogen synthase kinase 3 beta (GSK3β) via serine 9 phosphorylation. GSK3β inhibition stabilizes PPARα and enhances the transcription of genes linked to peroxisomal biogenesis (PEX3 and PEX5) and LD growth (Tip47). The effects of PIM1 on LD accumulation are abrogated with GW6471, a specific inhibitor for PPARα. Notably, LD accumulation downstream of PIM1 provides a significant survival advantage for prostate cancer cells during nutrient stress, such as glucose depletion. Inhibiting PIM reduces LD accumulation in vivo alongside slow tumor growth and proliferation. Furthermore, TKO mice, lacking PIM isoforms, exhibit suppression in circulating triglycerides. Overall, our findings establish PIM1 as an important regulator of LD accumulation through GSK3β-PPARα signaling axis to promote cell proliferation and survival during nutrient stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.