Evidence map›Paper›PMID 36617552›Full record

ArticleSignal transduction and targeted therapy2023

Blockade of NMT1 enzymatic activity inhibits N-myristoylation of VILIP3 protein and suppresses liver cancer progression.

Xiang-Peng Tan, Yan He, Jing Yang, Xian Wei, You-Long Fan, Guo-Geng Zhang, Yi-Dong Zhu, Zheng-Qiu Li, Hua-Xin Liao, Da-Jiang Qin and 2 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
13.8field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 60 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

12 authors at 5 institutions in 2 countries.

Xiang-Peng Tan *The First Affiliated Hospital of Jinan University, Jinan University, Guangzhou, China.
Yan He *Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes and Key Laboratory of Protein Modification and Degradation, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jing YangKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes and Key Laboratory of Protein Modification and Degradation, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xian WeiKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes and Key Laboratory of Protein Modification and Degradation, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
You-Long FanSchool of Pharmacy, Jinan University, Guangzhou, China.
Guo-Geng ZhangKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes and Key Laboratory of Protein Modification and Degradation, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Yi-Dong ZhuKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes and Key Laboratory of Protein Modification and Degradation, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Zheng-Qiu LiSchool of Pharmacy, Jinan University, Guangzhou, China.
Hua-Xin LiaoMOE Key Laboratory of Tumor Molecular Biology and National Engineering Research Center of Genetic Medicine, College of Life Science and Technology, Jinan University, Guangzhou, China.
Da-Jiang QinKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes and Key Laboratory of Protein Modification and Degradation, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xin-Yuan GuanDepartment of Clinical Oncology, The University of Hong Kong, Hong Kong, China.ORCID 0000-0002-4485-6017
Bin LiKey Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes and Key Laboratory of Protein Modification and Degradation, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. lib2128@163.com.ORCID 0000-0002-8979-610X
Jinan University · CNGuangzhou Medical University · CNChinese University of Hong Kong · HKFirst Affiliated Hospital of Jinan University · CNKey Laboratory of Guangdong Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. Identification of the underlying mechanism of HCC progression and exploration of new therapeutic drugs are urgently needed. Here, a compound library consisting of 419 FDA-approved drugs was taken to screen potential anticancer drugs. A series of functional assays showed that desloratadine, an antiallergic drug, can repress proliferation in HCC cell lines, cell-derived xenograft (CDX), patient-derived organoid (PDO) and patient-derived xenograft (PDX) models. N-myristoyl transferase 1 (NMT1) was identified as a target protein of desloratadine by drug affinity responsive target stability (DARTS) and surface plasmon resonance (SPR) assays. Upregulation of NMT1 expression enhanced but NMT1 knockdown suppressed tumor growth in vitro and in vivo. Metabolic labeling and mass spectrometry analyses revealed that Visinin-like protein 3 (VILIP3) was a new substrate of NMT1 in protein N-myristoylation modification, and high NMT1 or VILIP3 expression was associated with advanced stages and poor survival in HCC. Mechanistically, desloratadine binds to Asn-246 in NMT1 and inhibits its enzymatic activity, disrupting the NMT1-mediated myristoylation of the VILIP3 protein and subsequent NFκB/Bcl-2 signaling. Conclusively, this study demonstrates that desloratadine may be a novel anticancer drug and that NMT1-mediated myristoylation contributes to HCC progression and is a potential biomarker and therapeutic target in HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsHumansLoratadineMyristic AcidProtein Processing, Post-TranslationaldesloratadineLoratadineMyristic Acid

Identifiers

PMID36617552
PMCPMC9826789
OpenAlexW4313800178

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.