Evidence map›Paper›PMID 35486286›Full record

ArticleMolecular biology reports2022

Methylation-mediated silencing of miR-125a-5p facilitates breast cancer progression by inducing autophagy.

Fatemeh Ahmadpour, Somayeh Igder, Hossein Babaahmadi-Rezaei, Ehsan Khalili, Malek Kanani, Vahid Soleimani, Ghorban Mohammadzadeh

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Baicalin Relieves Airway Inflammation in COPD by Inhibiting miR-125a.Applied biochemistry and biotechnology · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. 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

7 authors at 3 institutions in 1 country.

Fatemeh AhmadpourDepartment of Clinical Biochemistry, School of Medicine, Cellular and Molecular Research Center, Medical Basic Science Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Somayeh IgderDepartment of Clinical Biochemistry, School of Medicine, Cellular and Molecular Research Center, Medical Basic Science Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Hossein Babaahmadi-RezaeiDepartment of Clinical Biochemistry, School of Medicine, Cellular and Molecular Research Center, Medical Basic Science Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Ehsan KhaliliDepartment of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Malek KananiDepartment of Pathology, Imam Khomeini Hospital, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Vahid SoleimaniDepartment of Pathology, Cancer Institute, Imam Khomeini Complex Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Ghorban MohammadzadehDepartment of Clinical Biochemistry, School of Medicine, Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. mohammadzadeh@ajums.ac.ir.ORCID http://orcid.org/0000-0001-7921-4770
Ahvaz Jundishapur University of Medical Sciences · IRImam Khomeini Hospital · IRTehran University of Medical Sciences · IR

Funding

Ahvaz Jundishapur University of Medical Sciences CMRC - 9710
6 · The paper itself

Abstract

backgroundmicroRNA-125a-5p (miR-125a) is a tumor suppressor gene whose role in autophagy remains poorly understood. In the current study, we aimed to investigate the methylation status of miR-125a, its transfection into SK-BR3 cells, and its effects on autophagy.

methodsSixty samples of tumor and non-tumor adjacent tissue were collected and the methylation status of miR-125a was evaluated by methylation-specific PCR (MSP). The effect of 5-Aza-dC on miR-125a expression was investigated in the SK-BR3 cells. Cells were also transfected with miR-125a mimic/antimiR. The expression of miR-125a and its target genes was evaluated by Real-Time PCR. Protein levels of ATG5 and LC3 were assessed by Western blotting. HER2 expression was investigated by immunocytochemistry (ICC).

resultsThe data showed that the miR-125a promoter CpG Island was significantly hypermethylated in breast cancer tissues (p < 0.01) and in SK-BR3 cells. The 5-Aza-dC could significantly increase miR-125a expression by decreasing its methylation (p < 0.05). In addition, Western blot analysis indicated the expression of ATG5 and LC3 II/ LC3I, as autophagy biomarkers, was significantly reduced in SK-BR3 cells transfected with miR-125a (p < 0.05).

conclusionsOur data showed miR-125a expression was significantly decreased in tumor tissues due to its promoter hypermethylation. Overexpression of miR-125a was associated with a reduction in autophagy, which could provide a new therapeutic avenue for advanced-stage breast cancer treatment.

Indexed as

Breast NeoplasmsMicroRNAsAutophagyCell Line, TumorCell ProliferationDNA MethylationFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsAutophagyBreast cancerMethylationmicroRNA-125a

Identifiers

PMID35486286
OpenAlexW4225146109

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.