AI Article Synopsis

  • * In CRC, let-7i-3p levels are significantly lower while CyclinD1 (CCND1) levels are higher, indicating a direct relationship between the two, with CCND1 being a target of let-7i-3p.
  • * Overexpressing let-7i-3p or silencing CCND1 can inhibit cancer cell growth and movement, suggesting that targeting let-7i-3p and CCND1 could provide new treatment options for CRC.

Article 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9175015PMC
http://dx.doi.org/10.1515/med-2022-0499DOI Listing

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