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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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Decreased PPM1B Expression Drives PRMT5-Mediated Histone Modification in Lung Cancer Progression.

Attila Makai1, Ilka Keller2, Fanni A Szalmás2

  • 1Health Care Service Units, Pulmonology Clinic, University of Debrecen Clinical Center, University of Debrecen, H-4032 Debrecen, Hungary.

Biomolecules
|November 27, 2025
PubMed
Summary
This summary is machine-generated.

Reduced PPM1B expression in lung cancer activates a carcinogenic pathway involving myosin phosphatase and PRMT5. This epigenetic dysregulation suppresses tumor suppressors, driving aggressive disease and indicating PPM1B as a prognostic marker.

Keywords:
adenocarcinomalung cancermethylationplanocellular carcinomaprotein arginine methyltransferase 5protein phosphatases

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Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Pulmonary carcinoma is an aggressive malignancy driven by complex signaling and epigenetic dysregulation.
  • The Mg2+/Mn2+-dependent protein phosphatase 1B (PPM1B) plays a role in cellular regulation.

Purpose of the Study:

  • To investigate the novel oncogenic PPM1B/myosin phosphatase (MP)/protein arginine methyltransferase 5 (PRMT5) axis in pulmonary carcinoma.
  • To determine the role of PPM1B in driving tumorigenesis and its potential as a prognostic marker.

Main Methods:

  • Western blotting, PCR, and immunohistochemistry were used to analyze protein and gene expression.
  • Expression levels of PPM1B, MYPT1 phosphorylation, PRMT5 phosphorylation, and histone H2A dimethylation were assessed.

Main Results:

  • PPM1B expression was significantly reduced in squamous cell carcinoma (SCC) and lung adenocarcinoma (ADC), correlating with poorer patient survival.
  • Inactivation of MP due to elevated inhibitory phosphorylation of MYPT1 and increased activating phosphorylation of PRMT5 were observed.
  • Elevated symmetric dimethylation of histone H2A led to decreased retinoblastoma protein expression, indicating epigenetic suppression of tumor suppressor genes.

Conclusions:

  • Decreased PPM1B expression drives oncogenic activation of the MP/PRMT5 axis, contributing to the aggressive nature of lung cancer, particularly SCC.
  • PPM1B serves as a potential prognostic marker for lung cancer, highlighting a novel therapeutic target.