Intermittent Fasting Reduces Taurine Availability and Promotes Antitumor Immunity Through PERK Attenuation-Associated Paraptosis-Like Cell Death in Colorectal Cancer.

Authors

Baohui Song, Sikei Kam, Jingyi Liu, Rui Lv, Xucheng Huo, Zhanghan Chen, Yuelun Dong, Shilun Cai, Bing Li, Ruobing Ren, Yunshi Zhong, Mingyan Cai

Published in

Advanced science (Weinheim, Baden-Wurttemberg, Germany). Pages e78107. Oct 06, 2026. Epub Oct 06, 2026.

Abstract

Intermittent fasting (IF) exerts antitumor activity in colorectal cancer (CRC), but the tumor-intrinsic metabolic mechanism linking nutrient restriction to antitumor immunity remains unclear. In this study, IF reduced taurine availability and suppressed tumor growth in a CD⁸⁺ T cell-dependent manner. Taurine supplementation attenuated this effect, whereas pharmacological inhibition of taurine uptake partially recapitulated fasting-associated tumor suppression in preclinical models. Mechanistically, taurine is associated with the endoplasmic reticulum chaperone GRP78 and contributes to the maintenance of PERK abundance under nutrient stress. As a metabolic consequence of IF, taurine restriction impaired PERK stability, suppressed downstream ERO1A signaling, and redirected CRC cells from stress tolerance toward paraptosis-like immunogenic stress. PERK loss enhanced CD⁸⁺ T-cell activation, remodeled the tumor microenvironment toward a less suppressive state, and supported tumor control in combination with anti-PD-1 therapy. The present study identified taurine restriction as a functional metabolic feature of IF that compromises PERK-dependent stress adaptation and promotes antitumor immunity in CRC.

PMID:
42839693
Bibliographic data and abstract were imported from PubMed on 07 Oct 2026.

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