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Which STAT partners dominate cancer signaling networks?

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An IID-based interactome shows STAT3 as the busiest hub, STAT1 as a frequent antagonist, and points to cytoplasmic nodes for JAK/STAT-targeted therapy ideas.

Source

JAK-STAT core cancer pathway: An integrative cancer interactome analysis

Erdogan F, Radu TB, Orlova A, et al. · Journal of cellular and molecular medicine · 2022

doi.org/10.1111/jcmm.17228Read the full paper ↗95 citationscc by

Study at a glance

Design
Computational / modelling — IID 2018 literature-curated STAT PPI interactomes filtered by disease/tissue expression context and visualized with NAViGaTOR
N
Network counts of STAT partners (e.g., STAT3 n=166 proteins) rather than a patient cohort N
Population
Curated human STAT protein–protein interactions across major cancer contexts
Outcome
Member-specific STAT interactomes and proposed targeting points in oncogenic JAK/STAT signaling

Structured fields used in claim comparison tables when every cited study has a complete layer.

Inspect source passages

Which STAT partners dominate cancer signaling networks?

These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.

What kind of analysis did the authors perform on STAT-linked disease data?

Through a comprehensive review and in silico analysis of reported data on STAT‐linked diseases

Which database supplied curated PPIs?

These data were collected using the integrated interactions database (IID) 2018 version
Read passages in the original paper

What they did

Using IID 2018 PPIs (stringent multi-evidence + expression context), the authors built global and cancer-specific STAT interactomes and mapped them with NAViGaTOR, integrating literature on STAT-linked diseases.

What they found

STAT3 had the largest diversity (166 partners) vs STAT1 (81); STAT3/5 emerge as pleiotropic oncogenes while STAT1 often counters STAT3; EGFR/ESR1 interplay and cytoplasmic hubs inform targeting hypotheses.

The limits

What it doesn't show

Not a clinical drug trial; missing edges may reflect study bias, and network centrality ≠ proven drug efficacy.

Key terms

JAK/STAT
Janus kinase / signal transducer and activator of transcription pathway.
Interactome
Network map of protein–protein interactions for STAT family members.
IID
Integrated Interactions Database supplying curated, context-annotated PPIs.
STAT3
Often oncogenic STAT with the largest interaction diversity in this analysis.
STAT1
Frequently antagonistic to oncogenic STAT3 in the authors’ framing.

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Common questions

Is this wet-lab binding for every edge?

No—it aggregates curated literature/database PPIs with expression filters.

Why STAT3 looks biggest?

Both biology and publication volume; authors note literature bias influences apparent degree.

Therapeutic takeaway?

Hitting central cytoplasmic communication hubs may limit pathway rerouting—hypothesis-generating.

Subject mapping?

Biology / cell-signaling (computational systems view of JAK/STAT).

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