Evidence map›Paper›PMID 39535362›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Integrin β8 Facilitates Macrophage Infiltration and Polarization by Regulating CCL5 to Promote LUAD Progression.

Lei Song, Xi Yu, Yang Wu, Wenwen Zhang, Yu Zhang, Yanchi Shao, Zhenxin Hou, Chen Yang, Yue Gao, Yanbin Zhao

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

40 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Lei SongDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Xi YuDepartment of Gynecological Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Yang WuDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Wenwen ZhangDepartment of Gynecological Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Yu ZhangDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Yanchi ShaoDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Zhenxin HouDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Chen YangDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.
Yue GaoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang, 150081, China.ORCID 0000-0003-0403-6783
Yanbin ZhaoDepartment of Internal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, China.ORCID 0000-0002-1350-8570

Funding

Harbin Medical University 0111-31021220041Harbin Medical University Cancer Hospital JJZD2023-02Harbin Medical University Cancer Hospital PDYS2024-01National Natura Science Foundation of China 32100528
6 · The paper itself

Abstract

The tumor microenvironment (TME) influences cancer progression and metastasis. Integrin β8 (ITGβ8), a member of the integrin family, is upregulated in various cancers. In this study, it is determined as a key factor that mediates the interaction between lung adenocarcinoma (LUAD) cells and macrophages. Increased expression levels of ITGβ8 are associated with increased numbers of CD163+ macrophages and poor prognosis in LUAD patients. The overexpression of ITGβ8 in LUAD cells promotes the polarization of THP-1 macrophages toward the M2 phenotype. In contrast, TCM (conditioned medium from the co-culture system) from THP-1 macrophages and ITGβ8-overexpressing A549 cells promoted the proliferation and invasion of A549 cells. Mechanistically, chemokine (C-C motif) ligand 5 (CCL5) plays an important role in mediating ITGβ8-induced macrophage polarization, and the phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase (AKT)/interferon regulatory factor 9 (IRF9) pathway is involved in this process. Moreover, interleukin 8 (IL8) and interleukin 10 (IL10) produced by M2-like macrophages regulate the expression of ITGβ8 in LUAD cells through the spi-1 proto-oncogene (SPI1). This study elucidates the feedback mechanism of ITGβ8 between LUAD cells and macrophages.

Indexed as

Adenocarcinoma of LungChemokine CCL5Integrin beta ChainsLung NeoplasmsMacrophagesA549 CellsCell Line, TumorCell ProliferationDisease ProgressionHumansProto-Oncogene MasTHP-1 CellsTumor MicroenvironmentCCL5 protein, humanChemokine CCL5integrin beta8Integrin beta ChainsMAS1 protein, humanProto-Oncogene MasCCL5ITGβ8LUADmacrophageTME

Identifiers

PMID39535362
PMCPMC11727125

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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.