Evidence map›Paper›PMID 41854744›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2026

Gsα deficiency in macrophages promotes tumor progression via the MAPK signaling pathway.

Wenjiang Yan, Jingjing Yang, Siyu Tan, Tixiao Wang, Rong Xiao, Na Li, Min Chen, Lee S Weinstein, Lifan He, Chang Ma and 6 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Wenjiang YanKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Jingjing YangDepartment of Emergency, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Siyu TanKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Tixiao WangKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Rong XiaoKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Na LiKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Min ChenMetabolic Diseases Branch, National Institute of Diabetes, National Institutes of Health, Digestive, and Kidney Diseases, Bethesda, MD, 20814, USA.
Lee S WeinsteinMetabolic Diseases Branch, National Institute of Diabetes, National Institutes of Health, Digestive, and Kidney Diseases, Bethesda, MD, 20814, USA.
Lifan HeNational Key Laboratory for Innovation and Transformation of Luobing Theory, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Chang MaNational Key Laboratory for Innovation and Transformation of Luobing Theory, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Jingsu ZhangNational Key Laboratory for Innovation and Transformation of Luobing Theory, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Lifen GaoKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Xiaohong LiangKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Xiaojia SongDepartment of Pharmacology, School of Medicine, University of Nevada, Reno, NV, 89557, USA. louis700@163.com.
Wencheng ZhangNational Key Laboratory for Innovation and Transformation of Luobing Theory, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, Shandong, China. zhangwencheng@sdu.edu.cn.
Chunhong MaKey Laboratory for Experimental Teratology of Ministry of Education and Department of Immunology, School of Basic Medical Sciences, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China. machunhong@sdu.edu.cn.ORCID http://orcid.org/0000-0002-8121-4718

Funding

National Natural Science Foundation of China 81902443National Natural Science Foundation of China 82270457National Natural Science Foundation of China 82470499Natural Science Foundation of Shandong Province ZR2024ZD23Taishan Scholar Project of Shandong Province of China tstp20240852
6 · The paper itself

Abstract

Under diverse stimuli in the tumor microenvironment, tumor-associated macrophages (TAMs) are susceptible to polarize toward an immunosuppressive phenotype. Reprogramming TAMs is a promising strategy for cancer immunotherapy. As a downstream molecule of G protein-coupled receptors, the alpha subunit of the stimulatory G protein (Gsα) plays an indispensable role in the transduction of extracellular signals to intracellular signals. However, whether Gsα is responsible for the reprogramming and polarization of TAMs is largely unknown. Here, we demonstrate that Gsα deficiency in TAMs accelerates tumor growth and metastasis in B16 and MC38 tumor cells. Further investigations revealed that Gsα upregulates the expression of CD86, CCR5, Il1b and Nos2 and inhibits CD206 and Il10 expression, which facilitates the recruitment and antitumoral activity of TAMs and contributes to the increased effector activity of CD8

Indexed as

MacrophagesMAP Kinase Signaling SystemTumor-Associated MacrophagesAnimalsCell Line, TumorDisease ProgressionFemaleHumansMiceMice, Inbred C57BLReceptors, CCR5Tumor MicroenvironmentReceptors, CCR5AntitumorGsαMAPKTAMs

Identifiers

What OpenQuestion holds

Textmetadata
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.