Evidence map›Paper›PMID 39992949›Full record

ArticlePloS one2025

Adaptation to acidic conditions that mimic the tumor microenvironment, downregulates miR-193b-3p, and induces EMT via TGFβ2 in A549 cells.

Sadayuki Higashi, Munekazu Yamakuchi, Hirohito Hashinokuchi, Kazunori Takenouchi, Akito Tabaru, Yoko Oyama, Chieko Fujisaki, Kiyonori Tanoue, Teruto Hashiguchi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

9 authors.

Sadayuki HigashiDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Munekazu YamakuchiDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.ORCID https://orcid.org/0000-0003-2181-7194
Hirohito HashinokuchiDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Kazunori TakenouchiDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Akito TabaruDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.ORCID https://orcid.org/0000-0001-6018-9974
Yoko OyamaDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Chieko FujisakiDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Kiyonori TanoueDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Teruto HashiguchiDepartment of Laboratory and Vascular Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acidic tumor microenvironment plays a critical role in the malignant transformation of cancer cells. One mechanism underlying this transformation involves epithelial-mesenchymal transition (EMT). This is induced by prolonged exposure to acidic conditions. EMT is an essential process in cancer progression, with Transforming Growth Factor Beta (TGF-β) playing a central role in its induction. However, little was known about the factors regulating TGF-β under acidic conditions. This study aimed to elucidate the mechanism of EMT under acidic conditions and identify novel therapeutic targets to inhibit cancer cell migration and metastasis. Focusing on lung cancer, we explored microRNAs associated with EMT that were differentially expressed under acidic conditions in A549 cells and identified miR-193b-3p as a novel candidate. Under acidic conditions, miR-193b-3p expression decreased around days 3-14. Downregulation of miR-193b-3p promoted increased TGFβ2 expression, resulting in EMT changes in A549 cells. Our study suggests that the interaction between miR-193b-3p, TGFβ2, and the acidic tumor microenvironment promotes cancer EMT change. Understanding these interactions may not only enhance our biological comprehension of cancer, but also pave the way for the development of targeted therapies to inhibit cancer metastasis.

Indexed as

Epithelial-Mesenchymal TransitionLung NeoplasmsMicroRNAsTransforming Growth Factor beta2Tumor MicroenvironmentA549 CellsCell MovementDown-RegulationGene Expression Regulation, NeoplasticHumansHydrogen-Ion ConcentrationMicroRNAsMIRN193 microRNA, humanTransforming Growth Factor beta2

Identifiers

PMID39992949
PMCPMC12140115

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Registered trials

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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.