ArticleCell death & disease2026
Circadian gene CLOCK-mediated LLPS of NBR1 and p62/SQSTM1 inhibits proliferation and migration of nasopharyngeal carcinoma.
Article in Cell death & disease, 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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Abstract
Circadian Locomotor Output Cycles Kaput (CLOCK) is a core circadian gene encoding a transcription factor essential for maintaining physiological rhythms, and has more recently been implicated in cancer biology. In this study, we uncover an unrecognized tumor-suppressive role of CLOCK in nasopharyngeal carcinoma (NPC). Mechanistically, CLOCK directly activates NBR1 transcription, leading to the stabilization of p62/SQSTM1 and the co-assembly of NBR1-p62 condensates via liquid-liquid phase separation (LLPS). These condensates serve as scaffolds for the recruitment of the E3 ubiquitin ligase TRIM38, which mediates the ubiquitination and proteasomal degradation of TAK1-binding protein 2 (TAB2), thereby attenuating NF-κB signaling. Functionally, this axis suppresses NPC cell proliferation and migration. Our findings reveal a novel CLOCK-NBR1/p62-TRIM38-TAB2 pathway that links circadian gene to LLPS-driven tumor suppression in NPC, providing new insights into the role of circadian genes in cancer biology and pointing to a potential therapeutic target for this malignancy.
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