Evidence map›Paper›PMID 30446635›Full record

ArticleCell death & disease2018

NMT1 inhibition modulates breast cancer progression through stress-triggered JNK pathway.

Lu Deng, Xinlei Gao, Bingjie Liu, Xueyan He, Jiahui Xu, Jiankun Qiang, Qingfa Wu, Suling Liu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 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 2 institutions in 2 countries.

Lu DengFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; Shanghai Medical College; Key Laboratory of Breast Cancer in Shanghai; Innovation Center for Cell Signaling Network; Cancer Institutes, Fudan University, 200032, Shanghai, China.
Xinlei GaoSchool of Life Science, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, Anhui, China.
Bingjie LiuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; Shanghai Medical College; Key Laboratory of Breast Cancer in Shanghai; Innovation Center for Cell Signaling Network; Cancer Institutes, Fudan University, 200032, Shanghai, China.
Xueyan HeFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; Shanghai Medical College; Key Laboratory of Breast Cancer in Shanghai; Innovation Center for Cell Signaling Network; Cancer Institutes, Fudan University, 200032, Shanghai, China.
Jiahui XuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; Shanghai Medical College; Key Laboratory of Breast Cancer in Shanghai; Innovation Center for Cell Signaling Network; Cancer Institutes, Fudan University, 200032, Shanghai, China.
Jiankun QiangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; Shanghai Medical College; Key Laboratory of Breast Cancer in Shanghai; Innovation Center for Cell Signaling Network; Cancer Institutes, Fudan University, 200032, Shanghai, China.
Qingfa WuSchool of Life Science, The CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, 230027, Hefei, Anhui, China.
Suling LiuFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; Shanghai Medical College; Key Laboratory of Breast Cancer in Shanghai; Innovation Center for Cell Signaling Network; Cancer Institutes, Fudan University, 200032, Shanghai, China. suling@fudan.edu.cn.ORCID http://orcid.org/0000-0002-0475-0242
Shanghai Medical College of Fudan University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myristoylation is one of key post-translational modifications that involved in signal transduction, cellular transformation and tumorigenesis. Increasing evidence demonstrates that targeting myristoylation might provide a new strategy for eliminating cancers. However, the underlying mechanisms are still yielded unclear. In this study, we demonstrated that genetic inhibition of N-myristoyltransferase NMT1 suppressed initiation, proliferation and invasion of breast cancer cells either in vitro or in vivo. We identified ROS could negatively regulate NMT1 expression and NMT1 knockdown conversely promoted oxidative stress, which formed a feedback loop. Furthermore, inhibition of NMT1 caused degraded proteins increase and ER stress, which cross-talked with mitochondria to produce more ROS. And both of oxidative stress and ER stress could activate JNK pathway, leading to autophagy which abrogated breast cancer progression especially triple-negative breast cancer (TNBC). These studies provide a preclinical proof of concept for targeting NMT1 as a strategy to treat breast cancer.

Indexed as

AcyltransferasesAnimalsAutophagyCell Line, TumorCell ProliferationDisease ProgressionEndoplasmic Reticulum StressFemaleGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMiceMyristic AcidNeoplasm InvasivenessProtein Processing, Post-TranslationalTriple Negative Breast NeoplasmsAcyltransferasesglycylpeptide N-tetradecanoyltransferaseMyristic Acid

Identifiers

PMID30446635
PMCPMC6240078
OpenAlexW2900866886

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.