AI Article Synopsis

  • The study investigates how miR-145-5p regulates ABRACL and its effects on the proliferation, migration, and invasion of esophageal carcinoma (EC) cells.
  • Methods used include gene expression analysis from TCGA, various bioinformatics tools for target prediction, and functional assays to assess the behavior of EC cells regarding miR-145-5p and ABRACL.
  • Results show that lower levels of miR-145-5p and higher levels of ABRACL are present in EC, with miR-145-5p negatively regulating ABRACL and thus influencing cancer cell behaviors, indicating its potential as a therapeutic target in EC treatment.

Article Abstract

Objective: The study is aimed at investigating the regulatory relationship between miR-145-5p and ABRACL, and has tried at clarifying the mechanisms underlying the proliferation, migration, and invasion of esophageal carcinoma (EC) cells.

Methods: Gene expression data related to EC were accessed from TCGA database, and the "edgeR" package was used to screen differentially expressed genes. TargetScan, miRDB, and miRTarBase databases were used to predict potential targets for the target miRNA miR-145-5p. qRT-PCR and Western blot were performed to assess the expression of miR-145-5p and ABRACL in EC cells. Dual-luciferase reporter assay was performed to validate the targeting relationship between miR-145-5p and ABRACL. Functional experiments including CCK-8 assay, Transwell migration, and invasion assays were used to detect the proliferation, migration, and invasion of EC cells.

Results: The expression of miR-145-5p was significantly decreased in EC, while ABRACL was remarkably increased. In addition, there was a negative correlation identified between miR-145-5p and ABRACL mRNA. Overexpressing miR-145-5p was able to suppress cell proliferation, migration, and invasion, whereas silencing miR-145-5p posed an opposite effect. In the meantime, ABRACL was identified as a direct target of miR-145-5p by dual-luciferase reporter assay. Furthermore, miR-145-5p could inhibit the expression of ABRACL, in turn inhibiting the proliferation, migration, and invasion of EC cells.

Conclusion: miR-145-5p functions on the proliferation, migration, and invasion of EC cells via targeting ABRACL, and it may be a novel therapeutic target in EC treatment.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7937467PMC
http://dx.doi.org/10.1155/2021/6692544DOI Listing

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