Evidence map›Paper›PMID 34895252›Full record

ReviewMolecular cancer2021

Crosstalk between autophagy and microbiota in cancer progression.

Yu Wang, Jiang Du, Xuemei Wu, Ahmed Abdelrehem, Yu Ren, Chao Liu, Xuan Zhou, Sinan Wang

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Autophagy in Melanoma: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Iranian journal of microbiology · 2025
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. The cancer microbiome.Advances in clinical chemistry · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024
    Review
  18. Article
  19. Review
  20. Review
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

8 authors at 4 institutions in 2 countries.

Yu Wang *Department of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China. wangyu1991@tmu.edu.cn.
Jiang Du *Department of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Xuemei Wu *Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin, China.
Ahmed AbdelrehemDepartment of Craniomaxillofacial and Plastic Surgery, Faculty of Dentistry, Alexandria University, Alexandria, Egypt.
Yu RenTianjin Research Center of Basic Medical Science, Tianjin Medical University, Tianjin, 300070, China.
Chao LiuDepartment of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China.
Xuan ZhouDepartment of Maxillofacial and Otorhinolaryngological Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, 300060, China. xuanzhou@tmu.edu.cn.
Sinan WangDepartment of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin, China. wangsinan@tmu.edu.cn.
Tianjin Medical University Cancer Institute and Hospital · CNTianjin Medical University · CNAlexandria University · EGTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a highly conserved catabolic process seen in eukaryotes and is essentially a lysosome-dependent protein degradation pathway. The dysregulation of autophagy is often associated with the pathogenesis of numerous types of cancers, and can not only promote the survival of cancer but also trigger the tumor cell death. During cancer development, the microbial community might predispose cells to tumorigenesis by promoting mucosal inflammation, causing systemic disorders, and may also regulate the immune response to cancer. The complex relationship between autophagy and microorganisms can protect the body by activating the immune system. In addition, autophagy and microorganisms can crosstalk with each other in multifaceted ways to influence various physiological and pathological responses involved in cancer progression. Various molecular mechanisms, correlating the microbiota disorders and autophagy activation, control the outcomes of protumor or antitumor responses, which depend on the cancer type, tumor microenvironment and disease stage. In this review, we mainly emphasize the leading role of autophagy during the interaction between pathogenic microorganisms and human cancers and investigate the various molecular mechanisms by which autophagy modulates such complicated biological processes. Moreover, we also highlight the possibility of curing cancers with multiple molecular agents targeting the microbiota/autophagy axis. Finally, we summarize the emerging clinical trials investigating the therapeutic potential of targeting either autophagy or microbiota as anticancer strategies, although the crosstalk between them has not been explored thoroughly.

Indexed as

AutophagyCell CommunicationHost Microbial InteractionsMicrobiotaAnimalsBiomarkersCell Transformation, NeoplasticClinical Trials as TopicDisease ManagementDisease ProgressionDisease SusceptibilityHumansMolecular Targeted TherapyNeoplasmsTreatment OutcomeBiomarkersAutophagyCancer progressionMicrobiotaTarget therapy

Identifiers

PMID34895252
PMCPMC8665582
OpenAlexW4200023475

What Socratic holds

Textmetadata
LicenceCC BY
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.