July 27, 2025Open Access

Glucose Metabolism Sustains Aberrant STAT3 Signaling in Colorectal Cancer via Glycosylated Paracrine Factors.

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Proteomic analysis shows glucose-dependent glycosylated proteins activate stat3 in colorectal cancer, indicating a new metabolic target.

Glucose metabolism sustains aberrant stat3 signaling in colorectal cancer by promoting tumor cell proliferation.
High basal stat3 activity leads to the production of glycosylated proteins, activating nearby cells via paracrine signaling.
Manipulating glucose levels revealed that both glucose and its metabolite GlcNAc are crucial for stat3 activation.
Inhibition of glycolysis significantly reduces stat3 activation and tumor growth in vivo, suggesting a therapeutic target.

Büscher et al. (2025) studied this question.

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