AI Article Synopsis

  • Long non-coding RNAs (lncRNAs) may play a key role in breast cancer tumorigenesis, with LINC01705 identified as a significant lncRNA through microarray analysis.
  • Various assays (like qRT-PCR, transwell, and wound-healing) showed that LINC01705 is highly expressed in breast cancer tissues and promotes cell migration and proliferation.
  • The study suggests that LINC01705 functions as a competing endogenous RNA (ceRNA) by binding to miR-186-5p, thereby regulating the expression of the translocated promoter region (TPR) in breast cancer.

Article Abstract

Long non-coding RNAs (lncRNAs) may be a regulatory factor of tumorigenesis. However, it is unclear what its biomechanisms are in breast cancer. In this study, different lncRNAs were detected in breast cancer through microarray analysis (GSE119233) and LINC01705 was selected for further study. qRT-PCR was then utilized for the detection of LINC01705 expression in breast cancer cells. A transwell assay, flow cytometry, 5-ethynyl-2'-deoxyuridine (EdU), a cell counting Kit-8 (CCK-8), and a wound-healing assay were performed to determine cell migration, invasion, apoptosis, and proliferation in breast cancer, respectively. For the identification of potential targets of LINC01705, dual-luciferase reporter gene and bioinformatics assays were conducted. Moreover, for the clarification of their interaction and roles in the regulation of the occurrence of breast cancer, Western blotting and RIP assays were conducted. Our findings revealed high LINC01705 expression in breast cancer tissues relative to adjacent non-cancerous tissues ( = 40, < 0.001). Overexpression of LINC01705 notably enhanced cell migration and proliferation in breast cancer. In addition, LINC01705 positively regulated the translocated promoter region, nuclear basket protein (TPR) through competition with miR-186-5p. In conclusion, our results suggest that LINC01705 is implicated in the progression of breast cancer via competitively binding to miR-186-5p as a competing endogenous RNA (ceRNA), thereby regulating TPR expression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412980PMC
http://dx.doi.org/10.3389/fgene.2020.00779DOI Listing

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