ArticleOpen medicine (Warsaw, Poland)2022
Let-7i-3p inhibits the cell cycle, proliferation, invasion, and migration of colorectal cancer cells via downregulating CCND1.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Dicer is essential for proper maturation, composition, and function in the postnatal retina.iScience · 2025Article
- VRK1/BANF1/GLI1 Axis Regulates Tumor Development and Progression of Colorectal Cancer.International journal of biological sciences · 2025Article
- Comprehensive profiling of extrachromosomal circular DNAs in colorectal cancer progression.Scientific reports · 2024Article
- Elucidation of the mechanism of action of ailanthone in the treatment of colorectal cancer: integration of network pharmacology, bioinformatics analysis and experimental validation.Frontiers in pharmacology · 2024Article
- Copper in the colorectal cancer microenvironment: pioneering a new era of cuproptosis-based therapy.Frontiers in oncology · 2024Review
- Dual mechanism of Let-7i in tumor progression.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated microRNAs are closely related to the malignant progression of colorectal cancer (CRC). Although abnormal let-7i-3p expression has been reported in various human cancers, its biological role and potential mechanism in CRC remain unclear. Therefore, the purpose of this study was to investigate the expression and regulation of let-7i-3p in CRC. Here, we demonstrated that let-7i-3p expression was significantly downregulated in three CRC cell lines while CyclinD1 (CCND1) was upregulated compared with the normal colon epithelial FHC cells. Moreover, bioinformatics and luciferase reporter assays revealed that CCND1 was a direct functional target of let-7i-3p. In addition, let-7i-3p overexpression or CCND1 silencing inhibited cell cycle, proliferation, invasion, and migration and diminished the activation of p-ERK in HCT116 cells. However, exogenously expressing CCND1 alleviated these effects. Taken together, our findings may provide new insight into the pathogenesis of CRC and let-7i-3p/CCND1 might function as new therapeutic targets for CRC.
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