Evidence map›Paper›PMID 36068649›Full record

ArticleJournal of extracellular vesicles2022

Extracellular vesicles from colorectal cancer cells promote metastasis via the NOD1 signalling pathway.

Xiduan Wei, Jingjia Ye, Yameng Pei, Chunting Wang, Hongzhen Yang, Jingyuan Tian, Guangxu Si, Yao Ma, Kun Wang, Gang Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of extracellular vesicles, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.9field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 47 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

10 authors at 4 institutions in 1 country.

Xiduan WeiSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.
Jingjia YeSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.
Yameng PeiSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.
Chunting WangSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.
Hongzhen YangSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.
Jingyuan TianSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.
Guangxu SiSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.
Yao MaInstitute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P. R. China.
Kun WangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Hepatobiliary and Pancreatic Surgery Unit I, Peking University Cancer Hospital & Institute, Beijing.
Gang LiuSchool of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.ORCID 0000-0001-5549-5686
Tsinghua University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CNYantai University · CN

Funding

National Natural Science Foundation of China 81273364National Natural Science Foundation of China 81703329National Natural Science Foundation of China 817731National Natural Science Foundation of China 81803358National Natural Science Foundation of China 82003568
6 · The paper itself

Abstract

Pattern-recognition receptors (PRRs) have been shown to promote tumour metastasis via sensing tumour cell-derived small extracellular vesicles (EVs). Nucleotide-binding oligomerisation domain 1 (NOD1), a cytoplasmic PRR, plays a role in colorectal cancer (CRC) by detecting bacterial products. However, the precise mechanisms underlying the effects of NOD1, following identification of CRC cell-derived EVs (CRC-EVs), to potentiate CRC liver metastasis (CRC-LM), remain poorly understood. Here, we demonstrate that CRC-EVs activate NOD1 in macrophages to initiate secretion of inflammatory cytokines and chemokines. NOD1-activated macrophages also promote CRC cell migration, while in a murine model of liver metastasis (LM), NOD1-deficient mice exhibit reduced metastasis following CRC-EV treatment. Furthermore, cell division cycle 42 (CDC42), a small Rho guanosine-5'-triphosphate (GTP)ase, is delivered by CRC-EVs into macrophages where it activates NOD1. In addition, EVs from the plasma of patients with CRC-LM mediate NOD1 activation in human peripheral blood mononuclear cells. Moreover, high NOD1 expression in tumour tissues is associated with poor prognosis of CRC-LM. Our findings suggest that CRC-EVs activate NOD1 to promote tumour metastasis, thus, NOD1 may serve as a potential target in the diagnosis and treatment of CRC-LM.

Indexed as

Colorectal NeoplasmsExtracellular VesiclesLiver NeoplasmsAnimalsHumansLeukocytes, MononuclearMiceNod1 Signaling Adaptor ProteinSignal TransductionNOD1 protein, humanNod1 Signaling Adaptor Proteincolorectal cancerextracellular vesiclesmetastatic liverNOD1 signalling

Identifiers

PMID36068649
PMCPMC9448875
OpenAlexW4294838681

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.