Evidence map›Paper›PMID 39996781›Full record

ArticleCells2025

Therapeutic Targeting of the Galectin-1/miR-22-3p Axis Regulates Cell Cycle and EMT Depending on the Molecular Subtype of Breast Cancer.

Ju Yeon Kim, Jun Ho Lee, Eun Jung Jung, Young Sim Son, Hee Jin Park, Jae Myung Kim, Taejin Park, Sang-Ho Jeong, Jinkwon Lee, Tae Han Kim and 2 more

Abstract read
In one paragraph

Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Healing mechanisms of Galectin-1 in the ischemic heart.Cell biochemistry and biophysics · 2026
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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

12 authors.

Ju Yeon KimDepartment of Surgery, Gyeongsang National University Hospital, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.
Jun Ho LeeDepartment of Surgery, Changwon Hanmaeun Hospital, Hanyang University College of Medicine, Changwon 51139, Republic of Korea.ORCID 0000-0002-1641-4772
Eun Jung JungInstitute of Health Science, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.ORCID 0000-0001-8413-613X
Young Sim SonInstitute of Health Science, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.
Hee Jin ParkDepartment of Surgery, Gyeongsang National University Hospital, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.
Jae Myung KimDepartment of Surgery, Gyeongsang National University Hospital, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.
Taejin ParkInstitute of Health Science, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.
Sang-Ho JeongInstitute of Health Science, Gyeongsang National University College of Medicine, Jinju 52727, Republic of Korea.ORCID 0000-0001-9061-6236
Jinkwon LeeDepartment of Surgery, Gyeongsang National University Changwon Hospital, Gyeongsang National University College of Medicine, Changwon 51472, Republic of Korea.
Tae Han KimDepartment of Surgery, Gyeongsang National University Changwon Hospital, Gyeongsang National University College of Medicine, Changwon 51472, Republic of Korea.
Seon Min LeeGyeongnam Bio-Health Research Support Center, Gyeongnam Branch Institute, Korea Institute of Toxicology (KIT), Jinju 52834, Republic of Korea.ORCID 0000-0001-8146-4971
Jeong Doo HeoGyeongnam Bio-Health Research Support Center, Gyeongnam Branch Institute, Korea Institute of Toxicology (KIT), Jinju 52834, Republic of Korea.

Funding

Biomedical Research Institute fund from the Gyeongsang National University Hospital GNUHCRF-2012-0010 and GNUHBRIF-2022-0009National Research Foundation of Korea (NRF) 2017R1D1A1B03034183, 2019R1F1A1057175, and RS-2023-00252701
6 · The paper itself

Abstract

Breast cancer is a highly heterogeneous disease; hence, it is crucial to understand its biology and identify new targets for the development of effective treatments. Galectin-1 is known to play an oncogenic role in breast cancer progression. It is known that oncogenic factors can influence cancer progression through interactions with miRNAs. The purpose of this study is to identify the clinical significance and biological role of galectin-1 and miR-22-3p in cancer progression according to the molecular subtype of breast cancer. We analyzed the expression of galectin-1 and miR-22-3p using cancer tissues and the correlation with clinical pathological characteristics. In addition, we investigated the regulation of the cell cycle and EMT processes of cancer progression through the galectin-1/miR-22-3p axis using cell lines of different breast cancer subtypes. miR-22-3p negatively regulates galectin-1 expression and the two molecules have opposite patterns of oncogenic and tumor-suppressive functions, respectively; furthermore, these two molecules are associated with metastasis-free survival. Cell experiments showed that miR-22-3p overexpression and galectin-1 knockdown inhibited the proliferation and invasion of breast cancer cells. Galectin-1 regulates different cancer progression pathways depending on the molecular subtype. In hormone receptor-positive breast cancer cells, galectin-1 knockdown mainly inhibited cell cycle-related substances and induced G0/G1 arrest, whereas in triple-negative breast cancer cells, it suppressed molecules related to the epithelial-mesenchymal transition pathway. In conclusion, the miR-22-3p/galectin-1 axis regulates different cancer metastasis mechanisms depending on the specific molecular subtype of breast cancer, and miR-22-3p/galectin-1 axis modulation may be a novel target for molecular subtype-specific personalized treatment.

Indexed as

Breast NeoplasmsCell CycleEpithelial-Mesenchymal TransitionGalectin 1MicroRNAsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansGalectin 1MicroRNAsMIRN22 microRNA, humanbreast cancercell cycleepithelial–mesenchymal transitiongalectin-1microRNA-22-3pmolecular type

Identifiers

PMID39996781
PMCPMC11854374

What OpenQuestion holds

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LicenceCC BY
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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.