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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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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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Updated: Aug 22, 2025

Semi-automatic PD-L1 Characterization and Enumeration of Circulating Tumor Cells from Non-small Cell Lung Cancer Patients by Immunofluorescence
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PD-L1 Activity Is Associated with Partial EMT and Metabolic Reprogramming in Carcinomas.

Srinath Muralidharan1, Manas Sehgal1, R Soundharya1

  • 1Centre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore 560012, India.

Current Oncology (Toronto, Ont.)
|November 10, 2022
PubMed
Summary
This summary is machine-generated.

Cancer immune evasion and metabolic reprogramming, driven by epithelial-mesenchymal transition (EMT), worsen patient outcomes. Enhanced PD-L1 activity and glycolysis correlate with poor survival, highlighting a synergistic effect in promoting metastasis and drug resistance.

Keywords:
glycolysisimmune checkpoint moleculesmeta-analysismetabolic plasticityoxidative phosphorylationpartial EMT

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Area of Science:

  • Oncology
  • Cancer Biology
  • Immunology

Background:

  • Immune evasion and metabolic reprogramming are key cancer hallmarks linked to poor prognosis and treatment resistance.
  • The interplay between immunosuppression and altered energy metabolism shapes the tumor microenvironment, promoting cancer aggressiveness.
  • A comprehensive pan-cancer analysis linking these hallmarks with epithelial-mesenchymal transition (EMT) was lacking.

Approach:

  • A meta-analysis of 184 transcriptomic datasets and The Cancer Genome Atlas (TCGA) data was performed.
  • Investigated the association between immune checkpoint markers (e.g., PD-L1) and metabolic signatures (glycolysis, OXPHOS) in relation to EMT.
  • Validated findings using single-cell RNA-seq and time-course EMT induction data.

Key Points:

  • Enhanced PD-L1 activity signatures positively correlate with partial EMT and elevated glycolysis, but reduced oxidative phosphorylation (OXPHOS) across numerous carcinomas.
  • These trends were consistently observed in both large-scale transcriptomic data and cell line experiments.
  • Concurrent enrichment of glycolysis and PD-L1 activity is associated with significantly worse overall survival compared to PD-L1 enrichment alone.

Conclusions:

  • Epithelial-mesenchymal transition (EMT) acts as a common driver linking immune evasion (PD-L1) and metabolic reprogramming (glycolysis).
  • Functional synergy between PD-L1 activity and glycolysis promotes cancer metastasis and multi-drug resistance.
  • Targeting these interconnected pathways may offer novel therapeutic strategies for advanced cancers.