ReviewCancer management and research2026
Context-Dependent Dual Roles of the Plexin-B Family in Cancer Progression: Mechanisms and Therapeutic Implications.
Review in Cancer management and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Plexin-B family, comprising Plexin-B1, Plexin-B2, and Plexin-B3, represents a class of single-pass transmembrane receptors whose context-dependent functional outputs are governed by six contextual determinants-ligand availability, co-receptor expression, downstream signaling state, cell type, microenvironmental cues, and disease stage-exhibiting striking functional duality in cancer progression. This review provides a comprehensive overview of the bidirectional regulatory mechanisms of Plexin-B receptors across multiple malignancies. This functional duality is exemplified by Plexin-B1, which promotes glioma invasion via RhoA/PI3K/AKT signaling yet suppresses early-stage melanoma progression through FAK/Rho inhibition; similarly, Plexin-B2 drives triple-negative breast cancer stemness while restricting skin cancer growth via YAP suppression. A central thesis of this review is that these six contextual determinants establish a framework for understanding receptor pleiotropy. Furthermore, while targeting Plexin-B signaling shows therapeutic promise (eg, pepinemab in clinical trials), indiscriminate inhibition risks abrogating tumor-suppressive functions and perturbing immune microenvironment homeostasis, underscoring the necessity for biomarker-driven stratification to prevent paradoxical oncogenic consequences.
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