Evidence map›Paper›PMID 33372604›Full record

ArticleCancer cell international2020

Intrahepatic cholangiocarcinoma induced M2-polarized tumor-associated macrophages facilitate tumor growth and invasiveness.

Hui Yuan, Zelong Lin, Yingjun Liu, Yuchuan Jiang, Ke Liu, Mengxian Tu, Nan Yao, Chen Qu, Jian Hong

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. 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
5.7field-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

43 citing papers in PubMed, 63 citations in OpenAlex.

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  13. Multiple-omics analysis reveals a dedifferentiation-immune loop in intrahepatic cholangiocarcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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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

9 authors at 4 institutions in 1 country.

Hui YuanDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510630, Guangdong, China.
Zelong LinCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510315, Guangdong, China.
Yingjun LiuDepartment of General Surgery, Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, 450008, Henan, China.
Yuchuan JiangCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510315, Guangdong, China.
Ke LiuCollege of Pharmacy, Jinan University, Guangzhou, 510632, Guangdong, China.
Mengxian TuDepartment of Oncology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, Guangdong, China.
Nan YaoDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510630, Guangdong, China.
Chen QuDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510630, Guangdong, China.
Jian HongDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, 510630, Guangdong, China. hongjian7@hotmail.com.ORCID http://orcid.org/0000-0003-1084-3979
Jinan University · CNTCM-Intigrated Cancer Center of Southern Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CNZhengzhou University · CN

Funding

National Natural Science Foundation of China 81672320National Natural Science Foundation of China 81802423National Natural Science Foundation of China 81871987Science and Technology Program of Guangzhou, China 201704020128Yangcheng Scholar Program 1201561579
6 · The paper itself

Abstract

backgroundM2-polarized tumor-associated macrophages (M2-TAMs) have been shown to correlate with the progression of various cancers, including intrahepatic cholangiocarcinoma (ICC). However, the interactions and mechanism between M2 macrophages and ICC are not completely clear. We aimed to clarify whether M2 macrophages promote the malignancy of ICC and its mechanism.

methodsTwo progressive murine models of ICC were used to evaluate the alterations in different macrophage populations and phenotypes. Furthermore, we assessed M2 macrophage infiltration in 48 human ICC and 15 normal liver samples. The protumor functions and the underlying molecular mechanisms of M2 macrophages in ICC were investigated in an in vitro coculture system.

resultsWe found that the number of M2 macrophages was significantly higher in ICC tissues than in normal bile ducts in the two murine models. M2 macrophage infiltration was highly increased in peritumoral compared with intratumoral regions and normal liver (p < 0.01). ICC cells induced macrophages to differentiate into the M2-TAM phenotype, and coculture with these M2 macrophages promoted ICC cell proliferation, invasion and epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, M2-TAM-derived IL-10 promoted the malignant properties of ICC cells through STAT3 signaling. Furthermore, blockade of IL-10/STAT3 signaling partly rescued the effects of M2 macrophages on ICC.

conclusionOur results indicated that M2-polarized macrophages induced by ICC promote tumor growth and invasiveness through IL-10/STAT3-induced EMT and might be a potential therapeutic target for ICC.

Indexed as

Epithelial–mesenchymal transitionIntrahepatic cholangiocarcinomaM2 macrophageSignal transducer and activator of transcription 3 (STAT3)

Identifiers

PMID33372604
PMCPMC7720384
OpenAlexW3111326311

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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.