Target intelligence / Profile preview

JMJD7-PLA2G4B readthrough fusion protein (JMJD7-PLA2G4B)

Target
JMJD7-PLA2G4B
Molecular classification
Fusion protein, Enzyme (contains portions of both a lysyl hydroxylase and phospholipase domain), Histone modification (from JMJD7), Other (readthrough transcription product)
01

Overview

JMJD7-PLA2G4B readthrough fusion protein is a naturally occurring fusion product of the neighboring genes JMJD7 (Jumonji domain-containing protein 7) and PLA2G4B (phospholipase A2, group IVB) detected in head and neck squamous cell carcinoma (HNSCC) and other tumor types. The fusion protein promotes cancer cell proliferation and survival by modulating cell cycle progression, AKT phosphorylation, and expression of key regulators such as SKP2, p21, and p27. Knockdown of the fusion transcript causes G1 arrest and increased apoptosis, suggesting its essential role in tumorigenesis. This fusion protein appears to function independently of the canonical JMJD7 or PLA2G4B proteins, implicating it as a novel oncogenic driver and a potential therapeutic target and biomarker in cancer, particularly HNSCC.

Other names
JMJD7-PLA2G4B fusionJMJD7-PLA2G4B readthrough transcriptJMJD7-PLA2G4B read-through
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Mechanism of action

Not directly targeted by drugs yet; possible actions would involve inhibition of the fusion protein’s ability to activate AKT phosphorylation and regulate SKP2, thus promoting cell cycle arrest and apoptosis in tumor cells

03

Biological functions

Cell cycle regulationCell proliferationApoptosis regulationRegulation of AKT phosphorylationRegulation of SKP2, p21, and p27 expression
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Disease associations

CancerSpecifically head and neck squamous cell carcinoma (HNSCC)Potentially roles in colon and breast cancer cell lines
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Safety considerations

As a recently discovered and cancer-specific fusion, direct therapeutic targeting may pose risks related to off-target effects or disruption of normal cell cycle regulation; specific safety data are not available
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Interacting drugs

None specifically reported for the fusion protein as of current knowledge; SKP2 and AKT pathway inhibitors are under investigation as indirect interactors
07

Biomarkers

Expression of JMJD7-PLA2G4B may serve as a prognostic marker for HNSCCAssociated changes in SKP2, p21, and p27 protein levels may act as downstream biomarkers

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