ORIGINAL RESEARCH ARTICLE

Long non-coding RNA DARS-AS1 facilitates breast cancer progression by modulating the miR-6835-3p/ATF3 axis

Krishnamoorthy Vignesh1* Pattusamy Thangamalar1
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1 Department of Noi Naadal, Government of Siddha Medical College, Tirunelveli, Tamil Nadu, India
CP 2024, 6(2), 2867
Submitted: 1 February 2024 | Accepted: 12 March 2024 | Published: 28 June 2024
© 2024 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

Long non-coding RNAs (lncRNAs) play crucial roles in various cellular processes associated with cancer progression, including invasion, proliferation, and metastasis. Despite this understanding, the specific role of DARS-AS1 in breast cancer remains underexplored. In this study, we employed quantitative reverse transcription-polymerase chain reaction to measure the expression levels of DARS-AS1 and miR-6835-3p. Functional assessments, including the cell invasion and CCK-8 assays, were conducted to investigate cellular behaviors. In addition, a luciferase reporter assay was employed to elucidate the mechanistic interaction between DARS-AS1 and miR-6835-3p. Notably, DARS-AS1 expression was elevated in breast cancer cell lines (MCF7 and MDA-MB-231) relative to the non-cancerous MCF-10A cells. Overexpression of DARS-AS1 enhanced cell growth and invasion in MDA-MB-231 breast cancer cells. Further investigation revealed that DARS-AS1 acts as a sponge for miR-6835-3p in breast cancer cells. Overexpression of miR-6835-3p inhibited luciferase activity, specifically in the presence of wild-type DARS-AS1, highlighting a direct interaction. Ectopic expression of DARS-AS1 suppressed miR-6835-3p in MDA-MB-231 cells. Concurrently, miR-6835-3p levels were downregulated in breast cancer cells, and miR-6835-3p exhibited a negative correlation with DARS-AS1 expression. Mechanistically, miR-6835-3p targeted ATF3 expression in breast cancer cells. Increased levels of DARS-AS1 were found to enhance cellular proliferation and invasion by modulating ATF3. Our findings indicate that DARS-AS1 acts as an oncogene in breast cancer, partially through regulation of the miR-6835-3p/ATF3 pathway. This study provides valuable insights into the molecular mechanisms contributing to breast cancer progression, offering potential targets for therapeutic interventions.

Keywords
miR-6835-3p
ATF3
LncRNA DARS-AS1
Breast cancer
Funding
No funds were received for this study.
Conflict of interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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