Jet lag-induced circadian disruption elevates glioma risk by altering molecular profiles in distinct brain regions.

ABSTRACT:

Purpose

To investigate the mechanism underlying chronic jet lag (CJL)-induced circadian disruption stimulating glioma-related gene expression across distinct brain regions, and to examine the regulatory role of core clock genes in modulating neural oncogenic susceptibility.

Methods

This experiment was initiated with the establishment of an animal model of CJL (6-h light-cycle advances every 2 days for 10 or 30 days) in wild-type and clock gene-deficient mice (Bmal1^-/-, Per1/2^-/-, and Cry1/2^-/-). Then, tissues harvested from six neural regions (i.e., hippocampus, prefrontal cortex, striatum, hypothalamus, raphe nuclei, and nucleus accumbens) were subjected to tissue-specific qPCR profiling of cancer-related genes (C-MYC, MDM-2, GADD45A, and p5

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC12297171 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature