Evidence map›Paper›PMID 37244966›Full record

ArticleScientific reports2023

Targeting long non-coding RNA MALAT1 reverses cancerous phenotypes of breast cancer cells through microRNA-561-3p/TOP2A axis.

Sara Hajibabaei, Nahid Nafissi, Yasamin Azimi, Reza Mahdian, Fatemeh Rahimi-Jamnani, Vahideh Valizadeh, Mohammad Hessam Rafiee, Masoumeh Azizi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. The Secret Life of NJournal of molecular biology · 2025
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  14. Long non-coding RNAs: Key regulators of stemness in breast cancer.Frontiers in cell and developmental biology · 2025
    Review
  15. Overexpression ofEuropean journal of breast health · 2024
    Article
  16. Review
  17. Article
  18. Review
  19. Genes · 2024
    Review
  20. Downregulation ofBiochemistry and biophysics reports · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Sara HajibabaeiMolecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, 69th Pasteur Street, Kargar Avenue, Tehran, Iran.
Nahid NafissiBreast Surgery Department, Iran University of Medical Sciences, Tehran, Iran.
Yasamin AzimiMolecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, 69th Pasteur Street, Kargar Avenue, Tehran, Iran.
Reza MahdianMolecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, 69th Pasteur Street, Kargar Avenue, Tehran, Iran.
Fatemeh Rahimi-JamnaniDepartment of Mycobacteriology and Pulmonary Research, Pasteur Institute of Iran, Tehran, Iran.
Vahideh ValizadehDepartment of Nano-Biotechnology, New Technologies Research Group, Pasteur Institute of Iran, Tehran, Iran.
Mohammad Hessam RafieeBlood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran.
Masoumeh AziziMolecular Medicine Department, Biotechnology Research Center, Pasteur Institute of Iran, 69th Pasteur Street, Kargar Avenue, Tehran, Iran. mazizi528@gmail.com.
Biotechnology Research Center · IRPasteur Institute of Iran · IRHigh Institute for Education and Research in Transfusion Medicine · IRIran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-coding RNAs, including Inc-RNA and miRNA, have been reported to regulate gene expression and are associated with cancer progression. MicroRNA-561-3p (miR-561-3p), as a tumor suppressor, has been reported to play a role in preventing cancer cell progression, and MALAT1 (Lnc-RNA) have also been demonstrated to promote malignancy in various cancers, such as breast cancer (BC). In this study, we aimed to determine the correlation between miR-561-3p and MALAT1 and their roles in breast cancer progression. The expression of MALAT1, mir-561-3p, and topoisomerase alpha 2 (TOP2A) as a target of miR-561-3p was determined in BC clinical samples and cell lines via qRT-PCR. The binding site between MALAT1, miR-561-3p, and TOP2A was investigated by performing the dual luciferase reporter assay. MALAT1 was knocked down by siRNA, and cell proliferation, apoptotic assays, and cell cycle arrest were evaluated. MALAT1 and TOP2A were significantly upregulated, while mir-561-3p expression was downregulated in BC samples and cell lines. MALAT1 knockdown significantly increased miR-561-3p expression, which was meaningfully inverted by co-transfection with the miR 561-3p inhibitor. Furthermore, the knockdown of MALAT1 by siRNA inhibited proliferation, induced apoptosis, and arrested the cell cycle at the G1 phase in BC cells. Notably, the mechanistic investigation revealed that MALAT1 predominantly acted as a competing endogenous RNA in BC by regulating the miR-561-3p/TOP2A axis. Based on our results, MALAT1 upregulation in BC may function as a tumor promoter in BC via directly sponging miRNA 561-3p, and MALAT1 knockdown serves a vital antitumor role in BC cell progression through the miR-561-3p/TOP2A axis.

Indexed as

MicroRNAsNeoplasmsRNA, Long NoncodingApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGenes, Tumor SuppressorRNA, Small InterferingMicroRNAsRNA, Long NoncodingRNA, Small Interfering

Identifiers

PMID37244966
PMCPMC10224942
OpenAlexW4378576060

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.