Role of the Circadian Clock GeneDEC1in Chemosensitivity and Apoptosis in Colorectal Cancer
Résumé fourni par la source
BACKGROUND/AIM: is related to the progression and recurrence of various types of cancer; however, its role in colorectal cancer has not been determined. Therefore, we aimed to evaluate the significance of DEC1 expression level in colorectal cancer and its relationship with prognosis. MATERIALS AND METHODS: Using quantitative reverse transcription-polymerase chain reaction and immunohistochemistry, we compared DEC1 mRNA and protein expression in clinical samples. We compared colorectal cancer cell lines and organoids using cell proliferation, wound healing, chemosensitivity, and apoptosis assays. We also performed RNA sequencing to investigate whether changes in DEC1 expression influence the expression of other genes, thereby affecting drug sensitivity and apoptosis. RESULTS: experiments revealed that DEC1 knockdown in colorectal cancer cell lines does not significantly affect cell proliferation or migration. Modulating DEC1 expression levels altered the sensitivity of cells to 5-fluorouracil, indicating that DEC1 plays a role in treatment response. The suppression of DEC1 expression led to an increase in cell apoptosis. RNA sequencing, analyses of data from The Cancer Genome Atlas database, and Metascape analysis revealed seven genes related to DEC1 associated with apoptosis. CONCLUSION: DEC1 expression is related to the circadian rhythm in colorectal cancer cells, and several other genes contribute to this relationship. Overall, DEC1 may function beyond circadian rhythm regulation, potentially affecting the development and progression of colorectal cancer.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé, mais le titre doit être comparé manuellement.
- Titre Crossref
- Role of the Circadian Clock Gene<i>DEC1</i>in Chemosensitivity and Apoptosis in Colorectal Cancer
- Date Crossref
- 27/05/2025
- Éditeur
- International Institute of Anticancer Research
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude et ne compte pas comme une seconde source scientifique indépendante.
Institutions déclarées
Une affiliation ne permet pas de déduire la nationalité d’un auteur.