Evidence map›Paper›PMID 36641471›Full record

ArticleJournal of translational medicine2023

M2 tumor-associated macrophage mediates the maintenance of stemness to promote cisplatin resistance by secreting TGF-β1 in esophageal squamous cell carcinoma.

Kaige Yang, Yufang Xie, Lele Xue, Fanping Li, Chenghua Luo, Weihua Liang, Haijun Zhang, Ya Li, Yilin Ren, Mengmeng Zhao and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Transcriptome analysis of key genes and pathways associated with cisplatin resistance in oral squamous cell carcinoma Cal27 cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  7. Review
  8. FERMT2 drives anoikis resistance and peritoneal metastasis by enhancing extracellular matrix deposition in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025
    Article
  9. Article
  10. Review
  11. MicroRNA-mediated autophagy regulation in thyroid cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025
    Review
  12. International journal of biological sciences · 2025
    Article
  13. Article
  14. Article
  15. Review
  16. TGF-β signaling: critical nexus of fibrogenesis and cancer.Journal of translational medicine · 2024
    Review
  17. Article
  18. Review
  19. Review
  20. Article
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

20 authors at 5 institutions in 2 countries.

Kaige Yang *Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Yufang Xie *Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Lele Xue *Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Fanping LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Chenghua LuoDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Weihua LiangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Haijun ZhangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Ya LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Yilin RenDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Mengmeng ZhaoDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Weinan WangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Jia LiuDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Xihua ShenDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Wenhu ZhouXiangya School of Pharmaceutical Sciences, Central South University, Changsha, 410013, Hunan, China.
Jing FeiDepartment of Medical Oncology, First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Weigang ChenDepartment of Gastroenterology, First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Wenyi GuAustralian Institute of Bioengineering and Nanotechnology, University of Queensland, Brisbane, Queensland, 4072, Australia.
Lianghai WangDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Feng LiDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China.
Jianming HuDepartment of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases (Ministry of Education)/Department of Pathology, the First Affiliated Hospital, Shihezi University School of Medicine, Xinjiang, 832002, China. hujianming@shzu.edu.cn.
Shihezi University · CNFirst Affiliated Hospital of Shihezi University Medical College · CNCapital Medical University · CNCentral South University · CNUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinoma (ESCC) is a deadly gastrointestinal malignancy, and chemotherapy resistance is a key factor leading to its poor prognosis. M2 tumor-associated macrophages (M2-TAMs) may be an important cause of chemoresistance in ESCC, but its exact mechanism is still unclear.

methodsIn order to study the role of M2-TAMs in ESCC chemoresistance, CCK-8, clone formation assay, flow cytometric apoptosis assay, qRT-PCR, western blotting, and serum-free sphere formation assays were used. In vivo animal experiments and human ESCC tissues were used to confirm the findings.

resultsIn vitro and in vivo animal experiments, M2-TAMs reduced the sensitivity of ESCC cells to cisplatin. Mechanistically, M2-TAMs highly secreted TGF-β1 which activated the TGFβR1-smad2/3 pathway to promote and maintain the stemness characteristic of ESCC cells, which could inhibit the sensitivity to cisplatin. Using TGFβ signaling inhibitor SB431542 or knockdown of TGFβR1 could reverse the cisplatin resistance of ESCC cells. In 92 cases of human ESCC tissues, individuals with a high density of M2-TAMs had considerably higher levels of TGF-β1. These patients also had worse prognoses and richer stemness markers.

conclusionTGF-β1 secreted from M2-TAMs promoted and maintained the stemness characteristic to induce cisplatin resistance in ESCC by activating the TGFβ1-Smad2/3 pathway.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaAnimalsCell Line, TumorCell ProliferationCisplatinHumansTransforming Growth Factor beta1Tumor-Associated MacrophagesCisplatinTransforming Growth Factor beta1Chemotherapy resistanceEsophageal squamous cell carcinomaStem cellTGF-β1Tumor-associated macrophage

Identifiers

PMID36641471
PMCPMC9840838
OpenAlexW4316114547

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.