ArticleScientific reports2018
Opposite Carcinogenic Effects of Circadian Clock Gene BMAL1.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 78 citations in OpenAlex.
- Role of the circadian rhythm in squamous cell carcinoma: From molecular mechanism to therapy (Review).Molecular medicine reports · 2026Review
- Biochemical mechanism of the mammalian circadian clock.FEBS letters · 2026Review
- Circadian rhythm and aryl hydrocarbon receptor crosstalk in bone marrow adipose tissue and implications in leukemia.Scientific reports · 2025Article
- Circadian rhythm disruption promotes M1 macrophages polarization exacerbating the inflammatory response in rosacea.Archives of dermatological research · 2025Article
- The mediating role of the TyG index in the relationship between circadian syndrome and cancer among middle-aged and elderly Chinese.BMC cancer · 2025Article
- Differential response of neurons to autophagy modulation in Huntington's disease.Autophagy reports · 2025Article
- Basic helix-loop-helix ARNT like 1 regulates the function of immune cells and participates in the development of immune-related diseases.Burns & trauma · 2025Review
- BMAL1 sex-specific effects in the neonatal mouse airway exposed to moderate hyperoxia.Physiological reports · 2024Article
- The interplay between the PI3K/AKT pathway and circadian clock in physiologic and cancer-related pathologic conditions.Cell proliferation · 2024Review
- BMAL1 collaborates with CLOCK to directly promote DNA double-strand break repair and tumor chemoresistance.Oncogene · 2023Article
- Major roles of the circadian clock in cancer.Cancer biology & medicine · 2023Review
- Circadian clock and lipid metabolism disorders: a potential therapeutic strategy for cancer.Frontiers in endocrinology · 2023Review
- Potential Role of the Circadian Clock in the Regulation of Cancer Stem Cells and Cancer Therapy.International journal of molecular sciences · 2022Review
- Discovery of a small molecule that selectively destabilizes Cryptochrome 1 and enhances life span in p53 knockout mice.Nature communications · 2022Article
- Article
- Disrupting Circadian Rhythm via the PER1-HK2 Axis Reverses Trastuzumab Resistance in Gastric Cancer.Cancer research · 2022Article
- Circadian and Immunity Cycle Talk in Cancer Destination: From Biological Aspects to In Silico Analysis.Cancers · 2022Review
- REGγ regulates circadian clock by modulating BMAL1 protein stability.Cell death discovery · 2021Article
- Roles of circadian clocks in cancer pathogenesis and treatment.Experimental & molecular medicine · 2021Review
- Structure-based design and classifications of small molecules regulating the circadian rhythm period.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The circadian clock confers daily rhythmicity on many biochemical and physiological functions and its disruption is associated with increased risks of developing obesity, diabetes, heart disease and cancer. Although, there are studies on the role of Bmal1 in carcinogenesis using germline, conditional or tissue-specific knockouts, it is still not well understood how BMAL1 gene affects cancer-related biological events at the molecular level. We, therefore, took an in vitro approach to understand the contribution of BMAL1 in this molecular mechanism using human breast epithelial cell lines by knocking out BMAL1 gene with CRISPR technology. We preferred epithelial cells over fibroblasts as the most of cancers originate from epithelial cells. After obtaining BMAL1 knockouts by targeting the gene at two different sites from non-tumorigenic MCF10A and invasive tumorigenic MDA-MB-231 cells, we analysed apoptosis and invasion properties of the cell lines as representative events in tumor development. BMAL1 disruption sensitized both cell lines to a bulky-DNA adduct forming agent (cisplatin) and a double-strand break-inducing agent (doxorubicin), while it enhanced the invasive properties of MDA-MB-231 cells. These results show that the disruption of clock genes may have opposing carcinogenic effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.