ArticleiScience2026
CTSZ-dependent anoikis resistance enhances malignant characters of glioblastoma via NF-κB signaling.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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9 authors.
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Abstract
Glioblastoma (GBM) remains one of the most aggressive and therapy-resistant malignancies of the central nervous system, with anoikis resistance emerging as a critical facilitator of tumor invasion and therapeutic failure. In this study, we identified cathepsin Z (CTSZ) as a pivotal regulator of anoikis resistance in GBM. Clinical data revealed significant elevation of CTSZ levels in GBM tissues, with its expression strongly correlating with adverse patient outcomes. Through comprehensive functional analysis, we determined that genetic knockdown of CTSZ substantially increased anoikis sensitivity in GBM cells while simultaneously attenuating multiple oncogenic characteristics. Mechanistically, we established that CTSZ-mediated anoikis resistance enhanced multiple malignant traits of GBM by activating nuclear factor kappa B (NF-κB) signaling, as evidenced by the impaired nuclear translocation of p65 following CTSZ-knockdown. Our findings collectively position the CTSZ/NF-κB axis as a crucial determinant of GBM pathogenesis and highlight CTSZ as a potential therapeutic target for this devastating disease.
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