Evidence map›Paper›PMID 37445705›Full record

ArticleInternational journal of molecular sciences2023

Microcystin-LR-Induced Interaction between M2 Tumor-Associated Macrophage and Colorectal Cancer Cell Promotes Colorectal Cancer Cell Migration through Regulating the Expression of TGF-β1 and CST3.

Xinying Jiang, Hailing Zhang, Hengshuo Zhang, Fan Wang, Xiaochang Wang, Tong Ding, Xuxiang Zhang, Ting Wang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 14 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 1 country.

Xinying JiangDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, China.
Hailing ZhangDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, China.
Hengshuo ZhangDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, China.
Fan WangDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, China.
Xiaochang WangDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, China.
Tong DingDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, China.
Xuxiang ZhangState Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Xianlin Campus, Nanjing University, Nanjing 210023, China.
Ting WangDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing 211166, China.ORCID 0000-0002-2425-4684
Nanjing Medical University · CNState Key Laboratory of Pollution Control and Resource Reuse · CN

Funding

National Natural Science Foundation of China 22176101National Natural Science Foundation of China 52025102
6 · The paper itself

Abstract

Microcystin-LR (MC-LR) is a toxic secondary metabolite produced by cyanobacteria that has been demonstrated to promote colorectal cancer (CRC). However, the mechanism by which MC-LR enhances CRC in the tumor microenvironment (TME) is poorly understood. To elucidate its role in TME, a co-culture system was established using CRC cells and M2 macrophages in a Transwell chamber. The study found that MC-LR promotes CRC cell migration by upregulating TGF-β1 expression and secretion in M2 macrophages and downregulating CST3 in CRC cells. Neutralizing TGF-β1 increased CST3 expression in CRC cells, while overexpressing CST3 in CRC cells suppressed TGF-β1 expression in M2 macrophages, both of which weakened MC-LR-induced cellular motility in the co-culture system. In vivo, the mice in the MC-LR/AOM/DSS group had more tumor nodules, deeper tumor invasion, and higher M2 macrophage infiltration compared to the AOM/DSS group, and the expression of TGF-β1 and CST3 in tumors was consistent with the cellular level. Overall, this study provides insights into the regulatory mechanism of MC-LR on TME, revealing that MC-LR upregulates the expression and secretion of TGF-β1 in M2 macrophages, which in turn inhibits the expression of CST3 in CRC cells to promote migration.

Indexed as

Colorectal NeoplasmsTransforming Growth Factor beta1AnimalsCell Line, TumorCell MovementMarine ToxinsMiceMicrocystinsTumor-Associated MacrophagesTumor Microenvironmentcyanoginosin LRMarine ToxinsMicrocystinsTransforming Growth Factor beta1colorectal cancerM2 tumor-associated macrophagesMC-LRmigrationTGF-β1

Identifiers

PMID37445705
PMCPMC10341441
OpenAlexW4382133428

What OpenQuestion holds

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LicenceCC BY
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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.