Evidence map›Paper›PMID 30988371›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2019

Autophagy-related 7 modulates tumor progression in triple-negative breast cancer.

Mingyang Li, Jingwei Liu, Sihui Li, Yanling Feng, Fei Yi, Liang Wang, Shi Wei, Liu Cao

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

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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

8 authors at 3 institutions in 3 countries.

Mingyang Li *Key Laboratory of Medical Cell Biology, Ministry of Education; Institute of Translational Medicine, China Medical University;, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, Shenyang, Liaoning Province, China.
Jingwei Liu *Key Laboratory of Medical Cell Biology, Ministry of Education; Institute of Translational Medicine, China Medical University;, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, Shenyang, Liaoning Province, China.
Sihui LiKey Laboratory of Medical Cell Biology, Ministry of Education; Institute of Translational Medicine, China Medical University;, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, Shenyang, Liaoning Province, China.
Yanling FengKey Laboratory of Medical Cell Biology, Ministry of Education; Institute of Translational Medicine, China Medical University;, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, Shenyang, Liaoning Province, China.
Fei YiKey Laboratory of Medical Cell Biology, Ministry of Education; Institute of Translational Medicine, China Medical University;, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, Shenyang, Liaoning Province, China.
Liang WangDepartment of pathology, The College of Basic Medical Science, China Medical University, Shenyang, Liaoning Province, China. cmuwangliang@qq.com.
Shi WeiSection of Surgical Pathology, Comprehensive Cancer Center, The University of Alabama at Birmingham, Birmingham, AL, USA. swei@uabmc.edu.
Liu CaoKey Laboratory of Medical Cell Biology, Ministry of Education; Institute of Translational Medicine, China Medical University;, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, Shenyang, Liaoning Province, China. lcao@cmu.edu.cn.
Ministry of Education of the People's Republic of China · CNChina Medical University · CNUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exact role of autophagy in breast cancers remains elusive. In this study, we explored the potential functions of autophagy-related 7 (Atg7) in breast cancer cell lines and tissues. Compared to normal breast tissue, a significantly lower expression of Atg7 was observed in triple-negative breast cancer (TNBC), but not other subtypes. A higher Atg7 expression was significantly associated with favorable clinicopathologic factors and better prognostic outcomes in patients with TNBC. Reflecting the clinical and pathologic observations, Atg7 was found to inhibit proliferation and migration, but promotes apoptosis in TNBC cell lines. Furthermore, Atg7 suppressed epithelial-mesenchymal transition through inhibiting aerobic glycolysis metabolism of TNBC cells. These findings provided novel molecular and clinical evidence of Atg7 in modulating the biological behavior of TNBC, thus warranting further investigation.

Indexed as

Triple Negative Breast NeoplasmsApoptosisAutophagy-Related Protein 7BreastCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleHumansMiddle AgedPrognosisAutophagy-Related Protein 7

Identifiers

PMID30988371
OpenAlexW2935781302

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.