Evidence map›Paper›PMID 37462772›Full record

ArticleJournal of cancer research and clinical oncology2023

A feed-forward loop based on aerobic glycolysis and TGF-β between tumor-associated macrophages and bladder cancer cells promoted malignant progression and immune escape.

Chengquan Shen, Jing Liu, Wei Jiao, Xuezhou Zhang, Xinzhao Zhao, Xuecheng Yang, Yonghua Wang

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

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  14. Myeloid cells meet CD8Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
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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

7 authors at 2 institutions in 1 country.

Chengquan Shen *Department of Urology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Qingdao, 266000, Shandong, People's Republic of China.
Jing Liu *Department of Research Management and International Cooperation, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Wei JiaoDepartment of Urology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Qingdao, 266000, Shandong, People's Republic of China.
Xuezhou ZhangDepartment of Urology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Qingdao, 266000, Shandong, People's Republic of China.
Xinzhao ZhaoDepartment of Urology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Qingdao, 266000, Shandong, People's Republic of China.
Xuecheng YangDepartment of Urology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Qingdao, 266000, Shandong, People's Republic of China. yangxuecheng@qdu.edu.cn.
Yonghua WangDepartment of Urology, The Affiliated Hospital of Qingdao University, No.16, Jiangsu Road, Qingdao, 266000, Shandong, People's Republic of China. wangyonghua@qdu.edu.cn.
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

National Natural Science Foundation of China 81972378
6 · The paper itself

Abstract

purposeImmunotherapy with programmed cell death 1/ligand 1 (PD-1/PD-L1) checkpoint inhibitors has revolutionized the systemic treatment of solid tumors, including bladder cancer. Previous studies have shown that enhanced glycolysis, tumor-associated macrophage (TAM) infiltration, and TGF-β secretion in the tumor microenvironment (TME) are closely related to PD-1/PD-L1 inhibitor immunotherapy resistance. However, the potential mechanism of their interaction in bladder cancer has not been fully uncovered.

methodsBy coculturing bladder cancer cells and TAMs, we studied the relationship and interaction mechanism between tumor cell glycolysis, TAM functional remodeling, TGF-β positive feedback secretion, and PD-L1 mRNA m6A methylation in the bladder cancer microenvironment.

resultsBioinformatics analysis and IHC staining found a close correlation between tumor glycolysis, M2 TAM infiltration, and the prognosis of bladder cancer patients. In Vitro experiments demonstrated that bladder cancer cells could re-educate M2 TAMs through lactate and promote TGF-β secretion via the HIF-1α signaling pathway. Reciprocally, in vitro, and in vivo experiments validated that M2 TAMs could promote glycolysis in bladder cancer cells by TGF-β via the Smad2/3 signaling pathways. Furthermore, M2 TAMs could also promote CSCs and EMT of bladder cancer cells. More importantly, we found M2 TAMs enhance PD-L1 mRNA m6A methylation by promoting METLL3 expression in bladder cancer via the TGF-β/Smad2/3 pathway in the TME.

conclusionsOur study highlights a feed-forward loop based on aerobic glycolysis and TGF-β between M2 TAMs and bladder cancer cells, which may be a potential mechanism of malignant progression and immunotherapy resistance in bladder cancer.

Indexed as

Bladder cancerGlycolysisPD-1/PD-L1 inhibitorTGF-βTumor-associated macrophage

Identifiers

PMID37462772
PMCPMC11798317
OpenAlexW4384626740

What OpenQuestion holds

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Registered trials

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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.