FCGBP Promotes Glioma Growth by Regulating JAK2/STAT3/c‐Myc Pathway

TL;DR

FCGBP promotes glioma growth by activating the JAK2/STAT3/c-Myc pathway and is linked to poor patient outcomes.

Contribution

This study identifies FCGBP as a novel driver of glioma progression through the JAK2/STAT3/c-Myc pathway.

Findings

FCGBP is overexpressed in glioma and correlates with higher tumor grades and poor prognosis.

FCGBP activates the JAK2/STAT3 pathway, increasing c-Myc levels to promote glioma cell aggressiveness.

HIF-1α enhances FCGBP expression in hypoxic tumor environments, further driving progression.

Abstract

FCGBP has been implicated in the development of a variety of tumors, but its exact role in glioma progression remains unclear.

This study utilized qRT‐PCR, Western blotting (WB), immunohistochemistry (IHC), and other techniques to assess FCGBP expression in glioma tissues. Additionally, various functional experiments were conducted to investigate its role in glioma progression. Animal models were employed to further elucidate the function of FCGBP, with a particular focus on its impact on the Janus Kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) signaling pathway.

The research findings indicated that FCGBP is significantly overexpressed in glioma and is closely associated with higher tumor grades and unfavorable clinical outcomes. Functional assays demonstrated that FCGBP promotes glioma cell aggressiveness by activating the JAK2/STAT3 signaling pathway.

This study highlights the critical role of FCGBP in glioma aggression and poor prognosis, indicating that it could serve as a potential therapeutic target.

Schematic representation of the proposed mechanism. FCGBP is highly expressed in gliomas and is negatively correlated with patient prognosis, contributing to glioma progression. Mechanistically, FCGBP promotes glioma progression through two key pathways: (1) FCGBP activates the JAK2‐STAT3 signaling pathway, leading to the upregulation of c‐Myc protein levels; (2) In the tumor’s hypoxic microenvironment, HIF‐1α directly binds to the FCGBP promoter, enhancing FCGBP protein expression.

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