ArticleMolecular medicine reports2017
Circadian gene hCLOCK contributes to progression of colorectal carcinoma and is directly regulated by tumor‑suppressive microRNA‑124.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Associations Between Chronotype, Genetic Susceptibility and Risk of Colorectal Cancer in UK Biobank.Journal of epidemiology and global health · 2025Article
- Epi-miRNAs: Regulators of the Histone Modification Machinery in Human Cancer.Journal of oncology · 2022Review
- MicroRNA-124 and microRNA-378 inhibit the proliferation and invasion of colorectal cancer by upregulating KiSS1.Translational cancer research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An abundance of studies has demonstrated that disruption of circadian rhythms is one of the factors that may contribute to the initiation and development of human colorectal carcinomas (CRCs). Recently, microRNA‑124 has been demonstrated to suppress tumor growth or metastasis of CRCs. However, the mechanisms of cross‑talk between microRNA‑124 (miR‑124) and circadian rhythms in the regulation of CRCs are poorly understood. The present study demonstrated that the protein expression levels of human circadian locomoter output cycles protein kaput (hCLOCK) is significantly increased, while miR‑124 is attenuated in high‑grade human CRC tissues and in the more invasive colorectal cancer cell lines SW620 and LOVO. It was further demonstrated that hCLOCK is a direct target of miR‑124. Upregulation of miR‑124 significantly inhibited hCLOCK expression in LOVO cells, and consequently inhibited its promoting effects on the proliferation and migration of LOVO cells. In conclusion, these data revealed that hCLOCK serves an enhancing role, whereas mir‑124 serves a suppressive role, in human CRC. Attenuation of miR‑124, of which hCLOCK is a direct target, leads to increased hCLOCK expression and disruption of circadian rhythms in CRC.
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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.