ArticleHistology and histopathology2020
LncRNA AY343892 inhibits breast cancer development by positively regulating BRCA1-mediated transcription of PTEN.
Article in Histology and histopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Defective Homologous Recombination Repair By Up-Regulating Lnc-HZ10/Ahr Loop in Human Trophoblast Cells Induced Miscarriage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- LINC01315 accelerates the growth and epithelial-mesenchymal transition of colorectal cancer cells via activating the Wnt/β-catenin signal.Bioengineered · 2022Article
- LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472.PeerJ · 2022Article
- Long noncoding RNA ZBED3-AS1 restrains breast cancer progression by targeting the microRNA-513a-5p/KLF6 axis.Thoracic cancer · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Breast cancer remains a major challenge despite dramatic advances in cancer research. The long non-coding RNA (lncRNA) has been reported to associate with carcinogenesis and progression of various cancers. In this research, we found that lncRNA AY343892 was significantly down-regulated in breast cancer tissues and cells. Besides, breast cancer patients with high AY343892 level exhibited a favorable prognosis. Functional assays indicated that overexpression of AY343892 significantly inhibited proliferation and promoted apoptosis in breast cancer cells. In terms of mechanism, PTEN and BRCA1 were confirmed to be regulated by AY343892 in breast cancer. Luciferase activity and chromatin immunoprecipitation (ChIP) assays indicated that AY343892 can regulate the promoter of PTEN by binding to BCRA1. Further investigation suggested that knockdown of AY343892 significantly promoted MDA-MB-231 cell proliferation and inhibited MDA-MB-231 cell apoptosis. However, these effects were reversed when PTEN was up-regulated. Moreover, PTEN silence can also countervail the inhibitory effect of overexpressed BCRA1 or AY343892 on the expressions of genes related to proliferation and apoptosis in breast cancer. In conclusion, this study illustrated that AY343892 inhibited breast cancer development by positively regulating BRCA1-mediated transcription of PTEN. This finding contributes to a better understanding in the pathogenesis of breast cancer and provides a theoretical basis for the treatment of breast cancer patients.
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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.