Evidence map›Paper›PMID 35796007›Full record

ArticleInternational journal of molecular medicine2022

Transcription factor KLF16 activates MAGT1 to regulate the tumorigenesis and progression of breast cancer.

Lin Li, Xi Zhang, Yuqi Li, Bo Xiao, Sibiao Pei, Hangyu Jiang, Xiaofen Zhang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  3. The Mechanism of MgInternational journal of molecular sciences · 2026
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  13. The KLF16/MYC feedback loop is a therapeutic target in bladder cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
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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

7 authors at 4 institutions in 1 country.

Lin Li *Key Laboratory for Biorheological Science and Technology of Ministry of Education, Bioengineering College of Chongqing University, Chongqing 400044, P.R. China.
Xi Zhang *Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, P.R. China.
Yuqi LiDepartment of Pharmacy, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan 637003, P.R. China.
Bo XiaoDepartment of Oncology, Nanchong Jialing District People's Hospital, Nanchong, Sichuan 637931, P.R. China.
Sibiao PeiDepartment of Pharmacy, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan 637003, P.R. China.
Hangyu JiangDepartment of Pharmacy, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan 637003, P.R. China.
Xiaofen ZhangDepartment of Oncology, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan 637003, P.R. China.
North Sichuan Medical University · CNSouthwest Hospital · CNChongqing University · CNNanchong Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the most frequent cause of cancer‑related mortality among women worldwide. The present study aimed to explore the role of magnesium transporter protein 1 (MAGT1) in breast cancer and to illustrate the potential underlying molecular mechanisms. Bioinformatic analysis was performed to explore the association between MAGT1 expression and patients with breast cancer. MTT, colony formation, wound healing and Transwell assays were performed to examine the proliferative, migratory and invasive abilities of MCF‑7 cells. Western blot analysis was conducted to determine the corresponding protein expression. Chromatin immunoprecipitation and luciferase reporter assays were carried out to reveal the interaction between MAGT1 and the Kruppel‑like factor 16 (KLF16). In addition, an experimental animal model was established by the subcutaneous injection of MCF‑7 cells into BALB/c nude mice, and tumor weight and size were measured. The results revealed that MAGT1 expression was upregulated in breast cancer. MAGT1 knockdown significantly suppressed the MCF‑7 cell proliferative, migratory and invasive abilities, and downregulated the protein expression of Ki67, proliferating cell nuclear antigen, MMP2 and MMP9. MAGT1 knockdown also markedly suppressed tumor growth

Indexed as

Breast NeoplasmsCation Transport ProteinsAnimalsCarcinogenesisCell MovementCell Transformation, NeoplasticFemaleHumansKruppel-Like Transcription FactorsMiceMice, NudeTranscription FactorsCation Transport ProteinsKLF16 protein, humanKruppel-Like Transcription FactorsMagT1 protein, humanTranscription Factorsbreast cancerinvasionKruppel‑like factor 16magnesium transporter protein 1proliferation

Identifiers

PMID35796007
PMCPMC9282640
OpenAlexW4284707837

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.