CRY1, Cryptochrome Circadian Regulator 1,

The study provides preliminary insight into the epigenetic effect of MMT. Future studies will have to confirm the DMPs, assess their impact on gene expression, and determine their clinical relevance.

TMEM5 is associated with circadian-gene expression patterns, temozolomide response, and bioenergetic readouts in GBM models. TMEM5 knockdown was accompanied by altered time-dependent expression profiles of multiple clock genes, reduced OCR/ECAR parameters under the tested conditions, and increased TMZ sensitivity. These findings support TMEM5 as a circadian-associated factor in GBM and provide a rationale for future studies to define whether TMEM5 directly influences circadian regulation and metabolic pathway remodeling in vivo.

We emphasize the associations between circadian disruption and CRC-including diagnostic markers, prognostic assessment, and chemosensitivity-and provide an in-depth discussion of chronotherapeutic strategies and their translational potential. Finally, we identify unaddressed scientific questions and propose future research directions to facilitate the development of novel targeted therapies for CRC.

Recent findings demonstrate that time-of-day-dependent administration of vaccines and immunotherapies, including checkpoint inhibitors, can significantly influence clinical efficacy and immune outcomes. Understanding the temporal orchestration of adaptive immunity thus holds translational potential for optimizing therapeutic strategies, including chronotherapy and vaccination scheduling.

Alterations in the protein expression levels of circadian clock genes may contribute to the development and behavior of PAs.

Additionally, such regulation requires DNA-PK-mediated phosphorylation of CRY1. Finally, this circadian regulation impacts cancer progression and response to radiation therapy of specific tumours.

Methylation analysis identified six CpG sites significantly associated with survival. In conclusion, EZH2 is a key regulator of HCC progression and potential prognostic biomarker and therapeutic target.

In contrast, preserving complex I function maintained adipogenic and metabolic gene networks and protected against diet- and circadian-induced metabolic dysfunction independently of weight gain. These findings reveal that circadian disruption impairs metabolic health through mitochondrial complex I dysfunction, establishing clock control of complex I as a key regulator of transcriptional and metabolic homeostasis.

These data indicate that circadian synchronization improves interpretability of BMAT-MSC molecular outputs and reveals disease-associated differences among HD, FA, and AML. This study is a preliminary investigation with limited sampling and timepoints; findings should be validated in larger cohorts with denser temporal resolution. Overall, the results provide a framework for integrating circadian context into BMAT-MSC analyses in health and hematological disease.

Finally, we found Cry1 depletion downregulated pro-apoptotic BAX and upregulated anti-apoptotic BCL2, while Cry1 overexpression produced the opposite effects, suggesting its role in apoptosis via the BCL2/BAX-mediated apoptosis pathway. These findings indicate that Cry1 acts as a tumor suppressor in HCC, providing insights into the circadian dysfunction-cancer pathogenesis connection and its potential as a diagnostic biomarker and therapeutic target requires further verification through preclinical and clinical investigations in the future.

However, further research is essential to clarify the underlying mechanisms and enable clinical application. By integrating foundational studies with clinical evidence, the present review provides a framework for chrono‑precision medicine in hepatology, while identifying current challenges and proposing strategies to accelerate the development and clinical implementation of circadian rhythm‑based therapies for liver disease.

This review summarizes the roles of CRY in chronic diseases and introduces therapeutic approaches using CRY-targeting compounds. A deeper understanding of the pathology of chronic diseases and the effects of CRY-targeting compounds may lead to new circadian clock-based strategies for clinical advances.