Evidence map›Paper›PMID 37237244›Full record

ArticleCellular and molecular life sciences : CMLS2023

G6PD activation in TNBC cells induces macrophage recruitment and M2 polarization to promote tumor progression.

Yin Li, Xiao Han, Zhoujun Lin, Changjun Wang, Zhenkun Fu, Qiang Sun, Chenggang Li

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  9. mCancer cell international · 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

7 authors at 3 institutions in 1 country.

Yin LiState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Xiao HanState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Zhoujun LinState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China.
Changjun WangDepartment of Breast Surgery, Peking Union Medical College Hospital, No.1 Shuaifuyuan, Dongcheng District, Beijing, 100730, China. wangchangjun@pumch.cn.
Zhenkun FuDepartment of Immunology, Wu Lien-Teh Institute, Heilongjiang Provincial Key Laboratory for Infection and Immunity, Harbin Medical University & Heilongjiang Academy of Medical Science, No.157 Baojian Street, Nangang District, Harbin, 150086, People's Republic of China. 300042@hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-8415-6533
Qiang SunDepartment of Breast Surgery, Peking Union Medical College Hospital, No.1 Shuaifuyuan, Dongcheng District, Beijing, 100730, China. sunqiangpumch@sina.com.
Chenggang LiState Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, No.38 Tongyan Road, Jinnan District, Tianjin, 300350, People's Republic of China. lichenggang@nankai.edu.cn.ORCID http://orcid.org/0000-0002-5551-6093
Nankai University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNHarbin Medical University · CN

Funding

State Key Laboratory of Medicinal Chemical Biology 2019014The Fundamental Research Funds for the Central Universities ZB19100128
6 · The paper itself

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) is involved in triple-negative breast cancer (TNBC) progression. Metabolic crosstalk between cancer cells and tumor-associated macrophages mediates tumor progression in TNBC. Molecular biological methods were applied to clarify the mechanism of the crosstalk between TNBC cells and M2 macrophages. In the present study, we verified that G6PD overexpression drives M2 macrophage polarization by directly combining with phospho-STAT1 and upregulating CCL2 and TGF-β1 secretion in TNBC cells. In turn, M2-like TAMs activated TNBC cells through IL-10 secretion, providing feedback to upregulate G6PD and promote TNBC cell migration and proliferation in vitro. Furthermore, we found that 6-AN (a specific inhibitor of G6PD) not only suppressed the cancer-driven polarization of macrophages toward the M2 phenotype but also inhibited the inherent M2 polarization of macrophages. Targeting the G6PD-regulated pentose phosphate pathway restrained TNBC progression and M2-type polarization of macrophages in vitro and in vivo.

Indexed as

Glucosephosphate DehydrogenaseTriple Negative Breast NeoplasmsCell Line, TumorHumansMacrophagesTumor MicroenvironmentG6PD protein, humanGlucosephosphate Dehydrogenase6-ANG6PDM2 macrophagesTNBC

Identifiers

PMID37237244
PMCPMC11073185
OpenAlexW4378515869

What Socratic 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 Socratic graph.